Record 1 of 44 - MEDLINE EXPRESS (R) 1/97-4/97 TI: Nitric oxide modulates arteriolar responses to increased sympathetic nerve activity. AU: Nase-GP; Boegehold-MA AD: Department of Physiology, West Virginia University School of Medicine, Morgantown 26506-9229, USA. SO: Am-J-Physiol. 1996 Sep; 271(3 Pt 2): H860-9 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0002-9513 PY: 1996 LA: ENGLISH CP: UNITED-STATES AB: The purpose of this study was to determine whether arteriolar responses to increased sympathetic nerve activity are limited by the actions of endogenous nitric oxide. Intravital microscopy was used to examine diameter responses of small feed arteries (SFA), first-order arterioles (1A) and second-order arterioles (2A) to perivascular sympathetic nerve stimulation in the superfused rat small intestine. Stimulation induced a frequency-dependent constriction in all vessel types that was completely abolished by the alpha-adrenoceptor antagonist phentolamine (10(-6) M). In SFA and 1A, the magnitude of sympathetic constriction was increased significantly in the presence of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine(L-NMMA, 10(-4) M). In SFA (n = 7), stimulation at 3, 8, and 16 Hz induced constrictions of 11 +/- 1, 28 +/- 4, and 42 +/- 3%, respectively, under the normal superfusate vs. 28 +/- 3, 46 +/- 5, and 76 +/- 3% in the presence of L-NMMA. For 1A (n = 7), stimulation induced constrictions of 10 +/- 1, 27 +/- 4, and 37 +/- 3% under the normal superfusate vs. 24 +/- 2, 47 +/- 3, and 72 +/- 4% in the presence of L-NMMA. The effect of L-NMMA on sympathetic constriction in SFA (n = 7) was completely reversed by the additional presence of 5 x 10(-3) M L-arginine in the superfusate. These results suggest that endogenous nitric oxide activity can attenuate sympathetic neurogenic constriction in the intestinal microvasculature. MESH: omega-N-Methylarginine-pharmacology; Electric-Stimulation; Enzyme-Inhibitors-pharmacology; Intestine,-Small-innervation; Rats-; Rats,-Sprague-Dawley; Sympathetic-Nervous-System-drug-effects; Vascular-Resistance; Vasomotor-System-physiology MESH: *Arterioles-physiology; *Nitric-Oxide-physiology; *Sympathetic-Nervous-System-physiology TG: Animal; In-Vitro; Male; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: HL44012HLNHLBI; HL52019HLNHLBI RN: 0; 10102-43-9; 17035-90-4 NM: Enzyme-Inhibitors; Nitric-Oxide; omega-N-Methylarginine AN: 97006023 UD: 9702 -------------------------------------------------------------------------------- Record 2 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Stimulation of lumbar sympathetic nerves may produce hindlimb vasodilation via the release of pre-formed stores of nitrosyl factors. AU: Davisson-RL; Shaffer-RA; Johnson-AK; Lewis-SJ AD: Cardiovascular Center, University of Iowa, Iowa City 52242, USA. SO: Neuroscience. 1996 Jun; 72(4): 881-7 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0306-4522 PY: 1996 LA: ENGLISH CP: UNITED-STATES AB: The physiological activation of lumbar sympathetic nerves by air-jet stress produces a hindlimb vasodilation in conscious rats. Although the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester markedly reduces the duration of this air-jet stress-induced vasodilation, it does not prevent the initial fall in resistance. These data suggest that the vasodilation is initiated by the release of an as yet unidentified factor, whereas the vasodilation is sustained by the release of nitric oxide or newly synthesized nitrosyl factors such as S-nitrosothiols. At present, the possibility that neurogenic vasodilation may be initiated by the release of pre-formed pools of nitrosyl factors from storage sites within the hindlimb vasculature has not been addressed. We reasoned that if nitrosyl factors do exist in storage pools, then we should be able to demonstrate a "use-dependent" loss of vasodilation after nitric oxide synthesis inhibition which would be the result of a gradual depletion of the releasable pools of these nitrosyl factors. In the present study, we examined the effects of repeated episodes of direct electrical stimulation of the lumbar sympathetic chain on ipsilateral hindlimb vascular resistance in pentobarbital-anesthetized rats prior to and following administration of the nitric oxide synthesis inhibitors N(G)-nitro-L-arginine methyl ester (10, 25 or 100 mumol/kg i.v.) or N(G)-nitro-L-arginine (50 mumol/kg i.v.). Three episodes of electrical stimulation of 3.2 +/- 0.4 V (20 Hz, 5 ms duration, 5 ms delay for 10 s given 5 min apart) produced pronounced and reproducible reductions in hindlimb vascular resistance in the ipsilateral hindlimb (-56 +/- 5%, -55 +/- 5% and -53 +/- 6%, respectively), but no changes in mean arterial pressure. Three episodes of electrical stimulation at 4.8 +/- 0.4 V also caused reproducible decreases in hindlimb resistance (-59 +/- 7%, -61 +/- 9% and -64 +/- 12%) and minor but reproducible decreases in blood pressure. The vasodilation produced by the first electrical stimulation at 3.2 +/- 0.4 V was completely abolished by a 25 mumol/kg dose of N(G)-nitro-L-arginine methyl ester (-11 +/- 9%). The initial episode of electrical stimulation at 4.8 +/- 0.4 V produced a pronounced fall in ipsilateral hindlimb resistance in the N(G)-nitro-L-arginine methyl ester-treated animals whereas the second and third stimulations produced progressively smaller vasodilations (-55 +/- 4%, -34 +/- 3% and -19 +/- 2%, respectively). The 10 mumol/kg dose of N(G)-nitro-L-arginine methyl ester was not effective whereas the 100 mumol/kg dose produced similar effects as the 25 mumol/kg dose. The 50 mumol/kg dose of N(G)-nitro-L-arginine produced similar effects as the higher doses of N(G)-nitro-L-arginine methyl ester. Those results suggest that lower intensity electrical stimulation of the lumbar sympathetic nerves produces vasodilation via the release of nitric oxide or newly synthesized nitrosyl factors such as S-nitrosothiols. In contrast, the vasodilation produced by higher intensity electrical stimulation may involve the mobilization and release of pre-formed pools of nitrosyl factors which undergo a "use-dependent" depletion in the absence of nitric oxide synthesis. These pre-formed pools of nitrosyl factors may exist within the sympathetic nerves themselves. In addition, they may be stored within the vascular endothelium and released by neurogenically-derived neurotransmitters/neuromodulators. MESH: Blood-Pressure-drug-effects; Electric-Stimulation; Enzyme-Inhibitors-pharmacology; Hindlimb-blood-supply; Hindlimb-physiology; Lumbosacral-Region-innervation; Nitroprusside-pharmacology; NG-Nitroarginine-Methyl-Ester-pharmacology; Rats-; Vasodilator-Agents-pharmacology MESH: *Adrenergic-Fibers-physiology; *Nitroso-Compounds-pharmacology; *Vasodilation-drug-effects TG: Animal PT: JOURNAL-ARTICLE RN: 0; 0; 0; 15078-28-1; 50903-99-6 NM: Enzyme-Inhibitors; Nitroso-Compounds; Vasodilator-Agents; Nitroprusside; NG-Nitroarginine-Methyl-Ester AN: 96323896 UD: 9701 -------------------------------------------------------------------------------- Record 3 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Effect of sodium nitroprusside on norepinephrine overflow and antidiuresis induced by stimulation of renal nerves in anesthetized dogs. AU: Maekawa-H; Matsumura-Y; Matsuo-G; Morimoto-S AD: Department of Pharmacology, Osaka University of Pharmaceutical Sciences, Matsubara, Japan. SO: J-Cardiovasc-Pharmacol. 1996 Feb; 27(2): 211-7 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0160-2446 PY: 1996 LA: ENGLISH CP: UNITED-STATES AB: To investigate the role of nitric oxide (NO) in the regulation of renal sympathetic nerve activity and renal function, we examined the effect of sodium nitroprusside (SNP), a NO donor, on renal actions induced by renal nerve stimulation (RNS) in anesthetized dogs, with or without blockade of an endogenous NO generation by NG-nitro-L-arginine (NOARG), a NO synthase inhibitor. Low-frequency RNS (0.5-2.0 Hz) enhanced the rate of norepinephrine secretion rate (NESR) from the kidney and decreased urine flow (UF), urinary excretion of sodium (U(Na)V), and fractional excretion of sodium (FENa, without affecting systemic and renal hemodynamics. The intrarenal arterial infusion of SNP, in a dose (1 mu g/kg/min) that does not affect renal hemodynamics and urine formation at the basal level, significantly attenuated the RNS-induced decreases in UF, UNa V and FENa. The intrarenal administration of NOARG (40 mu g/kg/min) elicited renal vasoconstriction and reduced urine formation. RNS during NOARG administration reduced renal blood flow (RBF) and glomerular filtration rate (GFR) and augmented RNS-induced reduction in urine formation. Simultaneously, NESR was markedly enhanced. The renal actions observed with NOARG administration during control and RNS periods were almost completely abolished by treatment with SNP. Therefore, we suggest that NO plays an important role in the regulation of renal function. Endogenous NO probably functions as an inhibitory modulator of renal noradrenergic neurotransmission at the prejunctional level. MESH: Adrenergic-Fibers-physiology; Brachial-Artery; Dogs-; Electric-Stimulation; Glomerular-Filtration-Rate; Hemodynamics-physiology; Natriuresis-drug-effects MESH: *Adrenergic-Fibers-drug-effects; *Diuresis-drug-effects; *Nitric-Oxide-physiology; *Nitroarginine-pharmacology; *Nitroprusside-pharmacology; *Norepinephrine-secretion; *Renal-Artery-innervation; *Vasodilator-Agents-pharmacology TG: Animal; Female; Male PT: JOURNAL-ARTICLE RN: 0; 10102-43-9; 15078-28-1; 2149-70-4; 51-41-2 NM: Vasodilator-Agents; Nitric-Oxide; Nitroprusside; Nitroarginine; Norepinephrine AN: 96361608 UD: 9701 -------------------------------------------------------------------------------- Record 4 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Use-dependent loss of active sympathetic neurogenic vasodilation after nitric oxide synthase inhibition in conscious rats. Evidence for the presence of preformed stores of nitric oxide-containing factors. AU: Davisson-RL; Shaffer-RA; Johnson-AK; Lewis-SJ AD: Cardiovascular Center, University of Iowa, Iowa City 52242, USA. SO: Hypertension. 1996 Sep; 28(3): 347-53 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0194-911X PY: 1996 LA: ENGLISH CP: UNITED-STATES AB: In this study, we examined whether air-jet stress-induced active sympathetic hindlimb vasodilation in conscious rats involves the release of preformed stores of nitric oxide-containing factors. We determined the effects of repeated episodes of air-jet stress (six episodes given 5 minutes apart) on mean arterial pressure and vascular resistances in the mesenteric bed and intact and sympathetically denervated hindlimb beds of conscious rats treated with saline or the nitric oxide synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 25 mumol/kg IV). In saline-treated rats, air-jet stress produced alerting behavior, minor changes in blood pressure, pronounced mesenteric vaso-constriction, and immediate and marked vasodilation in the sympathetically intact hindlimb but a minor vasodilation in the sympathetically denervated hindlimb. Each air-jet stress produced virtually identical responses. In L-NAME-treated rats, the first air-jet stress produced vasodilator responses in the sympathetically intact and sympathetically denervated hindlimbs that were similar to those in the saline-treated rats. However, each subsequent air-jet stress produced progressively smaller vasodilator responses in the sympathetically intact but not the sympathetically denervated hindlimb. There was no loss of air-jet stress-induced alerting behavior or mesenteric vasoconstriction, suggesting that L-NAME did not interfere with the central processing of the air-jet or the resultant changes in autonomic nerve activity. The progressive diminution of air-jet stress-induced vasodilation in the intact hindlimb of L-NAME-treated rats may be due to the use-dependent depletion of preformed stores of nitric oxide-containing factors that cannot be replenished in the absence of nitric oxide synthesis. MESH: Air-; Behavior,-Animal-physiology; Cysteine-analogs-and-derivatives; Cysteine-pharmacology; Hemodynamics-drug-effects; Hindlimb-blood-supply; Nitroprusside-pharmacology; Physical-Stimulation; Rats-; Rats,-Sprague-Dawley; Stress,-Mechanical MESH: *Nitric-Oxide-metabolism; *Nitric-Oxide-Synthase-antagonists-and-inhibitors; *NG-Nitroarginine-Methyl-Ester-pharmacology; *Sympathetic-Nervous-System-physiology; *Vasodilation-drug-effects; *Vasodilation-physiology TG: Animal; Male PT: JOURNAL-ARTICLE RN: EC 1.14.13.39; 10102-43-9; 15078-28-1; 4371-52-2; 50903-99-6; 51209-75-7 NM: Nitric-Oxide-Synthase; Nitric-Oxide; Nitroprusside; Cysteine; NG-Nitroarginine-Methyl-Ester; S-nitrosocysteine AN: 96387280 UD: 9701 -------------------------------------------------------------------------------- Record 5 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Effects of NO on baroreflex control of heart rate and renal nerve activity in conscious rabbits. AU: Liu-JL; Murakami-H; Zucker-IH AD: Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha 68198-4575, USA. SO: Am-J-Physiol. 1996 Jun; 270(6 Pt 2): R1361-70 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0002-9513 PY: 1996 LA: ENGLISH CP: UNITED-STATES AB: Recent data suggest that nitric oxide (NO) plays a role in the modulation of sympathetic nerve activity and baroreflex sensitivity. Most of these studies have been carried out in anesthetized preparations, and little if any comparison has been made on the relative role of NO on the baroreflex control of heart rate and sympathetic nerve activity. In the present studies, the effect of the NO synthase inhibitor NG-nitro-L-arginine (L-NNA) on the baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in conscious, instrumented rabbits. Intravenous bolus injections of 13 mg/kg of L-NNA decreased baseline HR (from 205.0 +/- 6.0 to 145.5 +/- 8.2 beats/min; P < 0.05) without significant changes in mean arterial pressure (MAP) and RSNA. L-NNA significantly reduced the lower plateau of the HR-MAP curves and increased the sensitivities of baroreflex control of HR and RSNA. L-Arginine (600 mg/kg i.v.) but not D-arginine reversed the above effects. The effects of L-NNA on baseline HR were not completely blocked by metoprolol (2 mg/kg) or by atropine (0.2 mg/kg). After pretreatment with metoprolol, baroreflex sensitivity was reduced and L-NNA increased baroreflex sensitivity back to the control level. After pretreatment with atropine, L-NNA still reduced the lower plateau but did not significantly affect baroreflex sensitivity. L-NNA increased the HR responses but not the RSNA response to electrical stimulation of the aortic nerve in chloralose-anesthetized, sinoaortic-denervated (SAD) rabbits. L-NNA had no effect on the HR response to right vagal stimulation. In both conscious intact and SAD rabbits, L-NNA did not increase baseline RSNA. These results suggest that endogenous NO decreases baroreflex control of HR and RSNA. Both sympathetic and parasympathetic components play a role in the effects of NO on the baroreflex control of HR. The effects of NO in the central nervous system play a more important role in the baroreflex control of HR than of RSNA. MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Autonomic-Nerve-Block; Baroreflex-drug-effects; Blood-Pressure-drug-effects; Central-Nervous-System-physiology; Denervation-; Electric-Stimulation; Enzyme-Inhibitors-pharmacology; Heart-Rate-drug-effects; Nitric-Oxide-Synthase-antagonists-and-inhibitors; Rabbits-; Sinus-of-Valsalva-innervation; Sympathetic-Nervous-System-drug-effects; Vagus-Nerve-physiology MESH: *Baroreflex-physiology; *Heart-Rate-physiology; *Kidney-innervation; *Nitric-Oxide-physiology; *Sympathetic-Nervous-System-physiology TG: Animal; Male; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: HL38690HLNHLBI RN: EC 1.14.13.39; 0; 10102-43-9; 2149-70-4; 7004-12-8 NM: Nitric-Oxide-Synthase; Enzyme-Inhibitors; Nitric-Oxide; Nitroarginine; Arginine AN: 96289260 UD: 9611 -------------------------------------------------------------------------------- Record 6 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Nitric oxide attenuates the renal hemodynamic responses to increased peripheral and renal sympathetic nerve activity. AU: Vogel-HW; Zambraski-EJ AD: Department of Biological Sciences, Rutgers University, Piscataway, New Jersey 08855, USA. SO: Proc-Soc-Exp-Biol-Med. 1996 Jul; 212(3): 263-70 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0037-9727 PY: 1996 LA: ENGLISH CP: UNITED-STATES AB: The role of nitric oxide (NO) in renal function was evaluated under conditions of elevated peripheral and renal sympathetic nerve activity (RSNA), achieved by bilateral carotid occlusion (CO) in anesthetized dogs. Renal function was monitored during CO with the NO system intact and with it blocked by the administration of L-NAME. With NO intact, CO increased arterial pressure and heart rate. With renal perfusion pressure held constant, CO also significantly decreased renal blood flow (RBF) and glomerular filtration rate (GFR) by 46% and 43%, respectively. CO, after L-NAME administration, resulted in a significantly exaggerated renal vasoconstriction. RBF and GFR decreased by 82% and 80%, respectively. Changes in water and sodium excretion were not different between the NO-intact and NO-blocked states during CO. These studies were also performed with the converting enzyme inhibitor, Captopril. The exaggerated renal hemodynamic responses to CO with NO synthesis inhibition were identical with or without Captopril. These findings indicate that under conditions of elevated peripheral and RSNA, NO plays an important role in modulating renal hemodynamics, but not sodium excretion. This effect does not appear to involve angiotensin II. MESH: Angiotensin-Converting-Enzyme-Inhibitors-pharmacology; Arginine-analogs-and-derivatives; Arginine-pharmacology; Captopril-pharmacology; Carotid-Arteries-surgery; Dogs-; Electrolytes-metabolism; Glomerular-Filtration-Rate-drug-effects; Kidney-drug-effects; Kidney-innervation; Nitric-Oxide-pharmacology; Renal-Circulation-drug-effects; Sympathetic-Nervous-System-drug-effects; Vasoconstriction-drug-effects MESH: *Nitric-Oxide-physiology; *Renal-Circulation-physiology; *Sympathetic-Nervous-System-physiology TG: Animal; Support,-U.S.-Gov't,-Non-P.H.S. PT: JOURNAL-ARTICLE RN: 0; 0; 10102-43-9; 50903-99-6; 62571-86-2; 7004-12-8 NM: Angiotensin-Converting-Enzyme-Inhibitors; Electrolytes; Nitric-Oxide; NG-Nitroarginine-Methyl-Ester; Captopril; Arginine AN: 96268354 UD: 9610 -------------------------------------------------------------------------------- Record 7 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Role of renal nerves in mediating the hypertensive effects of nitric oxide synthesis inhibition. AU: Granger-J; Novak-J; Schnackenberg-C; Williams-S; Reinhart-GA AD: Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505, USA. SO: Hypertension. 1996 Mar; 27(3 Pt 2): 613-8 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0194-911X PY: 1996 LA: ENGLISH CP: UNITED-STATES AB: Recent studies suggest that enhanced renal sympathetic nervous activity plays an important role in mediating the renal hemodynamic and electrolyte excretion changes associated with acute inhibition of NO synthesis. The purpose of this study was to determine the importance of renal nerves in mediating the long-term hypertensive and renal actions of NO synthesis blockade. To achieve this goal, we infused N(G)-nitro-L-arginine methyl ester (L-NAME) at a rate of 25 microg/kg per minute for 2 weeks in control dogs and in bilaterally renal-denervated dogs. NO synthesis blockade in control dogs increased arterial pressure by 18%, from 94 +/- 3 to 111 +/- 4 mm Hg, and decreased heart rate from 74 +/- 4 to 57 +/- 4 beats per minute (bpm). L-NAME also decreased renal plasma flow from 195 +/- 18 to 166 +/- 18 mL/min while having no effect on glomerular filtration rate (67 +/- 7 versus 63 +/- 6 mL/min). In the renal-denervated dogs, inhibition of NO synthesis increased arterial pressure by 14%, from 92 +/- 4 to 105 +/- 5 mm Hg, and decreased heart rate from 80 +/- 4 to 65 +/- 5 bpm. Renal plasma flow in this group decreased from 195 +/- 20 to 165 +/- 20 mL/min, whereas glomerular filtration rate remained unchanged (66+/- 6 versus 64 +/- 6 mL/min). In addition, renal excretion of sodium and water in response to L-NAME was similar in each group. The results of this study indicate that the long-term hypertensive and renal effects of NO synthesis inhibition in the dog are not dependent on activation of the renal sympathetic nervous system. MESH: Arginine-administration-and-dosage; Blood-Pressure; Denervation-; Dogs-; Hemodynamics-; Hypertension-etiology; Infusions,-Intra-Arterial; Infusions,-Intravenous; Kidney-physiopathology; Nitric-Oxide-antagonists-and-inhibitors MESH: *Arginine-analogs-and-derivatives; *Enzyme-Inhibitors-administration-and-dosage; *Hypertension-physiopathology; *Kidney-innervation; *Nitric-Oxide-physiology TG: Animal; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: HL51971HLNHLBI; HL33947HLNHLBI; HL09373HLNHLBI RN: 0; 10102-43-9; 50903-99-6; 7004-12-8 NM: Enzyme-Inhibitors; Nitric-Oxide; NG-Nitroarginine-Methyl-Ester; Arginine AN: 96188991 UD: 9608 -------------------------------------------------------------------------------- Record 8 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Axonal transport of nitric oxide synthase in autonomic nerves. AU: Lumme-A; Vanhatalo-S; Soinila-S AD: Department of Anatomy, University of Helsinki, Finland. SO: J-Auton-Nerv-Syst. 1996 Jan 5; 56(3): 207-14 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0165-1838 PY: 1996 LA: ENGLISH CP: NETHERLANDS AB: By using mechanical nerve ligation or nerve pinch technique, we provide evidence that nitric oxide synthase (NOS) is transported in the preganglionic sympathetic axons, while postganglionic axons lack NOS transport. This finding corroborates the preganglionic sympathetic terminal as the site of NO synthesis, which is known to affect ganglionic transmission. Both vasoactive intestinal polypeptide (VIP) and substance P (SP) containing neurons of the nodose ganglion transport NOS in their axons. These results therefore suggest that NOergic innervation of autonomically innervated tissues is of parasympathetic and/or sensory, rather than sympathetic, origin. MESH: Autonomic-Fibers,-Preganglionic-enzymology; Autonomic-Fibers,-Preganglionic-physiology; Autonomic-Nervous-System-cytology; Fluorescent-Antibody-Technique,-Indirect; Ganglia,-Parasympathetic-cytology; Ganglia,-Parasympathetic-enzymology; Ganglia,-Parasympathetic-physiology; Ganglia,-Sympathetic-cytology; Ganglia,-Sympathetic-enzymology; Ganglia,-Sympathetic-physiology; Ganglionectomy-; NADPH-Dehydrogenase-analysis; Parasympathetic-Fibers,-Postganglionic-enzymology; Parasympathetic-Fibers,-Postganglionic-physiology; Rats-; Rats,-Wistar; Substance-P-metabolism; Sympathetic-Fibers,-Postganglionic-enzymology; Sympathetic-Fibers,-Postganglionic-physiology; Vagus-Nerve-enzymology; Vagus-Nerve-physiology; Vasoactive-Intestinal-Peptide-metabolism MESH: *Autonomic-Nervous-System-enzymology; *Axonal-Transport-physiology; *Axons-enzymology; *Nitric-Oxide-Synthase-metabolism TG: Animal; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: EC 1.14.13.39; EC 1.6.99.1; 33507-63-0; 37221-79-7 NM: Nitric-Oxide-Synthase; NADPH-Dehydrogenase; Substance-P; Vasoactive-Intestinal-Peptide AN: 96401972 UD: 9612 -------------------------------------------------------------------------------- Record 9 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Relationship between sympathetic nervous system activity, baroreflex and cardiovascular effects after acute nitric oxide synthesis inhibition in humans. AU: Castellano-M; Rizzoni-D; Beschi-M; Muiesan-ML; Porteri-E; Bettoni-G; Salvetti-M; Cinelli-A; Zulli-R; Agabiti-Rosei-E AD: U.O.P. Scienze Mediche, University of Brescia, Italy. SO: J-Hypertens. 1995 Oct; 13(10): 1153-61 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0263-6352 PY: 1995 LA: ENGLISH CP: ENGLAND AB: OBJECTIVE: To examine the cardiovascular effects of acute systemic nitric oxide synthesis inhibition in humans in relation to the possible involvement of changes in sympathetic nervous system activity or in the baroreceptor reflex. DESIGN: Placebo or NG-monomethyl-L-arginine (250 mg by intravenous infusion for 5 min) was administered to seven healthy male volunteers according to a random, double-blind sequence. METHODS: Blood pressure and heart rate were measured non-invasively using a Finapres device from 20 min before to 80 min after starting infusion; beat-to-beat variability of blood pressure, pulse interval and systolic blood pressure and pulse interval covariation were assessed by means of spectral and sequence analysis methods. Under basal conditions and 15 min and 60 min after infusion, we measured stroke volume and indices of cardiac systolic and diastolic function by echocardiography, forearm blood flow by strain-gauge venous occlusion plethysmography, and plasma catecholamine levels. RESULTS: Compared with placebo, administration of NG-monomethyl-L-arginine caused a transient increase in blood pressure and reduction in heart rate. Stroke volume and indices of cardiac function did not change significantly, whereas cardiac index and forearm blood flow were significantly reduced after 15 min. Spectral analysis of blood pressure and pulse interval showed a significant reduction of power spectral density in the low frequencies (0.03-0.15 Hz) that persisted 60 min after infusion. The plasma noradrenaline level was significantly reduced after 15 min. No change in baroreflex engagement or sensitivity was detected by the cross-spectral or the sequence method. CONCLUSIONS: Acute systemic nitric oxide synthesis inhibition transiently increases blood pressure and reduces heart rate and cardiac index. The acute hypertensive response to NG-monomethyl-L-arginine is dependent neither on sympathetic nervous system activity, which is probably reduced as a consequence of baroreceptor reflex activation, nor on baroreceptor reflex sensitivity, which is not impaired. MESH: Adult-; Arginine-analogs-and-derivatives; Arginine-pharmacology; Cardiovascular-System-metabolism; Cardiovascular-System-physiology; Catecholamines-blood; Echocardiography-; Enzyme-Inhibitors-pharmacology; Nitric-Oxide-antagonists-and-inhibitors; Sympathetic-Nervous-System-metabolism MESH: *Baroreflex-physiology; *Cardiovascular-System-innervation; *Hemodynamics-physiology; *Nitric-Oxide-biosynthesis; *Sympathetic-Nervous-System-physiology TG: Human; Male PT: JOURNAL-ARTICLE RN: 0; 0; 10102-43-9; 17035-90-4; 7004-12-8 NM: Catecholamines; Enzyme-Inhibitors; Nitric-Oxide; omega-N-Methylarginine; Arginine AN: 96162516 UD: 9605 -------------------------------------------------------------------------------- Record 10 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Nitric oxide and peripheral adrenergic neuromodulation. AU: Levi-R; Park-KH; Imamura-M; Seyedi-N; Lander-HM AD: Department of Pharmacology, Cornell University Medical College, New York, New York 10021, USA. SO: Adv-Pharmacol. 1995; 34: 399-413 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 1054-3589 PY: 1995 LA: ENGLISH CP: UNITED-STATES MESH: Antihypertensive-Agents-pharmacology; Arginine-analogs-and-derivatives; Arginine-pharmacology; Electric-Stimulation; Enzyme-Inhibitors-pharmacology; Guinea-Pigs; Heart-drug-effects; Heart-physiology; Mesenteric-Arteries-metabolism; Mesenteric-Arteries-physiology; Myocardial-Reperfusion-Injury-drug-therapy; Myocardial-Reperfusion-Injury-physiopathology; Nitric-Oxide-Synthase-antagonists-and-inhibitors; Nitroprusside-pharmacology; Norepinephrine-blood; Rats-; Rats,-Sprague-Dawley; Synaptic-Transmission-drug-effects; Synaptosomes-drug-effects; Synaptosomes-metabolism MESH: *Nitric-Oxide-physiology; *Peripheral-Nervous-System-physiology; *Sympathetic-Nervous-System-physiology TG: Animal; In-Vitro; Male; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: HL34215HLNHLBI; HL46403HLNHLBI RN: EC 1.14.13.39; 0; 0; 10102-43-9; 15078-28-1; 17035-90-4; 51-41-2; 7004-12-8 NM: Nitric-Oxide-Synthase; Antihypertensive-Agents; Enzyme-Inhibitors; Nitric-Oxide; Nitroprusside; omega-N-Methylarginine; Norepinephrine; Arginine AN: 96126159 UD: 9605 -------------------------------------------------------------------------------- Record 11 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Effects of nitric oxide on sympathetic baroreflex transmission in the nucleus tractus solitarii and caudal ventrolateral medulla in cats. AU: Zanzinger-J; Czachurski-J; Seller-H AD: I. Physiologisches Institut, Universitat Heidelberg, Germany. SO: Neurosci-Lett. 1995 Sep 15; 197(3): 199-202 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0304-3940 PY: 1995 LA: ENGLISH CP: IRELAND AB: We have previously shown that nitric oxide (NO) attenuates baseline sympathetic tone in the rostral ventrolateral medulla (RVLM), while having no effects on baroreflex transmission in this region in cats. In the present study, we tested the effects of microinjections (500 nl) of NG-nitro-L-arginine (L-NNA, 0.3 mM) or the NO donor S-nitroso-N-acetylpenicillamine (SNAP, 10 microM) in the nucleus tractus solitarii (NTS) and in the caudal ventrolateral medulla (CVLM) which are the two other relays of the sympathetic baroreflex within the brainstem. Neither L-NNA nor SNAP significantly changed the length of inhibition of renal sympathetic nerve activity (SNA) evoked by electrical stimulation of the ipsilateral carotid sinus nerve. In contrast, glutamate (1 mM) in the NTS markedly increased baroreflex inhibition of SNA and the glutamate receptor antagonist kynurenate (5 mM) in the CVLM significantly decreased baroreflex transmission in the same experiments. These results suggest that sympathetic baroreflex function is preserved during both impaired endogenous synthesis and excess exogenous supply of NO in the brainstem. MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Baroreflex-drug-effects; Carotid-Sinus-physiology; Cats-; Electric-Stimulation; Glutamic-Acid-pharmacology; Kidney-innervation; Kynurenic-Acid-pharmacology; Neural-Inhibition-drug-effects; Nitric-Oxide-Synthase-antagonists-and-inhibitors; Penicillamine-analogs-and-derivatives; Penicillamine-pharmacology; Sympathetic-Nervous-System-drug-effects; Synaptic-Transmission-drug-effects MESH: *Baroreflex-physiology; *Medulla-Oblongata-physiology; *Nitric-Oxide-physiology; *Sympathetic-Nervous-System-physiology; *Synaptic-Transmission-physiology TG: Animal; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: EC 1.14.13.39; 10102-43-9; 2149-70-4; 492-27-3; 52-67-5; 56-86-0; 7004-12-8; 79032-48-7 NM: Nitric-Oxide-Synthase; Nitric-Oxide; Nitroarginine; Kynurenic-Acid; Penicillamine; Glutamic-Acid; Arginine; S-nitroso-N-acetylpenicillamine AN: 96117194 UD: 9604 -------------------------------------------------------------------------------- Record 12 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Differential sympathetic nerve responses to nitric oxide synthase inhibition in anesthetized rats. AU: Hirai-T; Musch-TI; Morgan-DA; Kregel-KC; Claassen-DE; Pickar-JG; Lewis-SJ; Kenney-MJ AD: Department of Anatomy and Physiology, Kansas State University, Manhattan 66506, USA. SO: Am-J-Physiol. 1995 Oct; 269(4 Pt 2): R807-13 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0002-9513 PY: 1995 LA: ENGLISH CP: UNITED-STATES AB: Recent studies have suggested that the interaction between the sympathetic nervous system and nitric oxide (NO) or nitrosyl factors may be an important means by which arterial blood pressure is regulated. We investigated whether NO synthase (NOS) inhibition modulates basal sympathetic nerve discharge (SND) in baroreceptor-innervated and -denervated, chloralose-anesthetized Sprague-Dawley rats. We recorded mean arterial pressure (MAP), renal SND, and lumbar SND before and after administration of the NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg iv). Two minutes after L-NAME administration in baroreceptor-innervated rats, MAP increased (+23 +/- 3 mmHg), whereas renal (-45 +/- 6%, n = 7) and lumbar (-35 +/- 2%, n = 6) SND significantly decreased from control levels. These changes persisted for up to 20 min after L-NAME administration. In baroreceptor-denervated rats, L-NAME increased MAP (+40 +/- 6 mmHg) and decreased lumbar SND (n = 7) (-37 +/- 10% from control at 20 min post-L-NAME). In contrast, renal SND progressively increased (+33 +/- 8% at 20 min post-L-NAME) from control after L-NAME administration in baroreceptor-denervated rats (n = 7). These results demonstrate that NOS inhibition can produce nonuniform changes in SND in baroreceptor-denervated rats and suggest that endogenous nitrosyl factors provide tonic excitation to lumbar SND, whereas they provide a tonic restraint to renal SND. MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Arteries-innervation; Blood-Pressure-drug-effects; Denervation-; Heart-Rate-drug-effects; Kidney-innervation; Lumbosacral-Region; Pressoreceptors-physiology; Rats-; Rats,-Sprague-Dawley MESH: *Nitric-Oxide-Synthase-antagonists-and-inhibitors; *Sympathetic-Nervous-System-physiology TG: Animal; Male; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: HL48564HLNHLBI; AG11535AGNIA; AG12350AGNIA RN: EC 1.14.13.39; 50903-99-6; 7004-12-8 NM: Nitric-Oxide-Synthase; NG-Nitroarginine-Methyl-Ester; Arginine AN: 96043492 UD: 9602 -------------------------------------------------------------------------------- Record 13 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Sympathetically mediated hypertension caused by chronic inhibition of nitric oxide. AU: Sander-M; Hansen-PG; Victor-RG AD: Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-8573, USA. SO: Hypertension. 1995 Oct; 26(4): 691-5 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0194-911X PY: 1995 LA: ENGLISH CP: UNITED-STATES AB: Pharmacological inhibition of nitric oxide synthase causes sustained hypertension in many animal species. Although this hypertension has been attributed to inhibition of endothelium-dependent vasodilation, short-term studies in anesthetized preparations have advanced the hypothesis that there could be a sympathetic component to this hypertension. To test this hypothesis we measured intra-arterial pressure directly before and after 1 week of treatment with the nitric oxide synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, approximately 80 mg/kg per day in drinking water) in conscious unrestrained rats with or without chronic guanethidine-induced sympathectomy. The major new finding is that the hypertensive response to L-NAME was greatly attenuated by sympathectomy. With L-NAME, mean arterial pressure increased from 101 +/- 3 to 152 +/- 6 mm Hg in rats without sympathectomy (n = 11) but only from 96 +/- 2 to 122 +/- 3 mm Hg in rats with sympathectomy (n = 15, +52 +/- 5 versus +27 +/- 4 mm Hg, P < .01). Sympathectomy did not alter maximal endothelium-dependent vasodilation assessed by femoral vascular responses to intra-arterial acetylcholine or bradykinin, indicating that the differing hypertensive responses to L-NAME in rats with versus without sympathectomy could be related to inhibition of neuronal rather than endothelial nitric oxide synthesis. We also found that L-NAME-induced hypertension, once developed, is completely reversed by acute ganglionic blockade. In conclusion, these findings identify an important sympathetic neural component to the sustained hypertension produced by pharmacological inhibition of nitric oxide in the rat. MESH: Acetylcholine-pharmacology; Arginine-analogs-and-derivatives; Arginine-pharmacology; Blood-Pressure-drug-effects; Bradykinin-pharmacology; Chlorisondamine-pharmacology; Femoral-Artery-drug-effects; Rats-; Rats,-Sprague-Dawley; Sympathectomy-; Time-Factors MESH: *Hypertension-etiology; *Nitric-Oxide-antagonists-and-inhibitors; *Sympathetic-Nervous-System-physiology TG: Animal; Female; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 10102-43-9; 50903-99-6; 51-84-3; 58-82-2; 69-27-2; 7004-12-8 NM: Nitric-Oxide; NG-Nitroarginine-Methyl-Ester; Acetylcholine; Bradykinin; Chlorisondamine; Arginine AN: 96035951 UD: 9601 -------------------------------------------------------------------------------- Record 14 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Endogenous and exogenous nitric oxide inhibits norepinephrine release from rat heart sympathetic nerves. AU: Schwarz-P; Diem-R; Dun-NJ; Forstermann-U AD: Department of Pharmacology, Johannes Gutenberg University, Mainz, Germany. SO: Circ-Res. 1995 Oct; 77(4): 841-8 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0009-7330 PY: 1995 LA: ENGLISH CP: UNITED-STATES AB: This study was designed to elucidate whether nitric oxide (NO) controls norepinephrine (NE) release from sympathetic nerves of the rat heart. Hearts were perfused in the Langendorff mode with Tyrode's solution. The right sympathetic nerve was stimulated with trains of 1 or 3 Hz and NE release was measured. The NO synthase (NOS) inhibitor NG-nitro-L-arginine (L-NNA) enhanced the evoked NE release in a concentration-dependent manner. This facilitation was independent of the increase in perfusion pressure and was stereospecifically reversed by L-arginine but not D-arginine. Another NOS inhibitor, NG-methyl-L-arginine, produced a similar increase in NE release. The NO-donor compound S-nitroso-N-acetyl-D,L-penicillamine, added in the presence of L-NNA, restored the suppression of NE release in a concentration-dependent fashion. A similar suppression was achieved with 3-morpholinosydnonimine. These results demonstrated that NE release is under the inhibitory control of endogenous NO. Western blots demonstrated the presence of neuronal NOS I and endothelial NOS III in the hearts. Perfusion of the hearts with a low concentration of the detergent CHAPS produced functional damage of the endothelium, as evidenced by an increase in perfusion pressure and a conversion of the acetylcholine-induced coronary vasodilation to a constriction. However, CHAPS treatment did not produce a facilitation of NE release (as did the NOS inhibitors), and L-NNA still increased NE release in CHAPS-treated hearts. Double-labeling immunofluorescence histochemistry showed NOS I immunoreactivity in stellate ganglion cells and in neurons of the heart, some of which also stained positive for tyrosine hydroxylase.(ABSTRACT TRUNCATED AT 250 WORDS) MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Enzyme-Inhibitors-pharmacology; Immunohistochemistry-; Nitric-Oxide-Synthase-analysis; Rats-; Rats,-Sprague-Dawley MESH: *Heart-innervation; *Nitric-Oxide-metabolism; *Norepinephrine-secretion; *Sympathetic-Nervous-System-metabolism TG: Animal; Female; In-Vitro; Male; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: NS18710NSNINDS; NS24226NSNINDS RN: EC 1.14.13.39; 0; 10102-43-9; 17035-90-4; 51-41-2; 7004-12-8 NM: Nitric-Oxide-Synthase; Enzyme-Inhibitors; Nitric-Oxide; omega-N-Methylarginine; Norepinephrine; Arginine AN: 96032299 UD: 9601 -------------------------------------------------------------------------------- Record 15 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Enhancement of the vasoconstrictor response to KCL by nitric oxide synthesis inhibition: a comparison with noradrenaline. AU: Amerini-S; Mantelli-L; Ledda-F AD: Department of Pharmacology, University of Florence, Italy. SO: Pharmacol-Res. 1995 Mar-Apr; 31(3-4): 175-81 ISSN: 1043-6618 PY: 1995 LA: ENGLISH CP: ENGLAND AB: The role of the vascular endothelium in the response to a vasoconstrictor agent acting through a non-receptorial mechanism, such as KCl, was tested in the isolated mesenteric vascular bed of the rat. It was confirmed that the vasoconstrictor response evoked by stimulation of sympathetic terminals was unaffected by 100 microM NG-nitro-D-arginine methyl ester (D-NAME), but was significantly potentiated by 100 microM NG-nitro-L-arginine methyl ester (L-NAME) and by removal of endothelium. Responses to exogenous noradrenaline (1-100 microM) were also enhanced by treatment with 100 microM NG-monomethyl-L-arginine (L-NMMA) and with L-NAME, but not with D-NAME. The potentiating effect of NO synthesis inhibitors was reversed by 1 mM L-arginine. Moreover, the noradrenaline-induced vasoconstriction was significantly increased by endothelium-deprivation. Potassium chloride (80 mM) induced a vasoconstrictor response which was not modified by pretreatment with prazosin (0.1 microM) and yohimbine (0.1 microM). The response to KCl was unaffected by D-NAME (100 microM) but the L-stereoisomer induced a significant increase in the perfusion pressure. In endothelium-denuded preparations the vasoconstrictor response to KCl was greater than in control conditions and was quantitatively similar to that observed in L-NAME-treated preparations. The responses to electrical field stimulation, noradrenaline and KCl in endothelium-denuded preparations were not modified by L-NAME. The results suggest that an increase in vascular tone, per se, may represent a trigger for the release of endothelium-derived relaxing factor from endothelial cells. MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Endothelium,-Vascular-physiology; Rats-; Rats,-Wistar; Sympathetic-Nervous-System-physiology MESH: *Amino-Acid-Oxidoreductases-antagonists-and-inhibitors; *Nitric-Oxide-physiology; *Norepinephrine-pharmacology; *Potassium-Chloride-pharmacology; *Vasoconstriction-drug-effects TG: Animal; Comparative-Study; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: EC 1.14.13.39; EC 1.4.; 10102-43-9; 17035-90-4; 50903-99-6; 51-41-2; 7004-12-8; 7447-40-7 NM: Nitric-Oxide-Synthase; Amino-Acid-Oxidoreductases; Nitric-Oxide; omega-N-Methylarginine; NG-Nitroarginine-Methyl-Ester; Norepinephrine; Arginine; Potassium-Chloride AN: 95357292 UD: 9511 -------------------------------------------------------------------------------- Record 16 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Effects of chronic NO synthase inhibition in rats on renin-angiotensin system and sympathetic nervous system. AU: Zanchi-A; Schaad-NC; Osterheld-MC; Grouzmann-E; Nussberger-J; Brunner-HR; Waeber-B AD: Hypertension Division, University Hospital, Lausanne, Switzerland. SO: Am-J-Physiol. 1995 Jun; 268(6 Pt 2): H2267-73 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0002-9513 PY: 1995 LA: ENGLISH CP: UNITED-STATES AB: This study was designed to assess the role of renin and of the sympathoadrenal system in the maintenance of the hypertension induced by chronic nitric oxide synthase (NOS) inhibition in rats kept on a normal (RS) or a low-sodium (LS) diet. With the administration of NG-nitro-L-arginine methyl ester (L-NAME) in drinking water (0.4 milligrams) for 6 wk, mean intra-arterial blood pressure rose to a similar extent to 201 mmHg in the RS and 184 mmHg in the LS animals. Simultaneously, plasma norepinephrine was increased to 838 and 527 pg/ml and epinephrine to 2,041 and 1,341 pg/ml in RS and LS, respectively. Plasma neuropeptide Y levels did not change. Plasma renin activity rose to 21 ng.ml-1.h-1 in RS but remained at 44 ng.ml-1.h-1 in the LS. Both losartan (10 mg/kg) and phentolamine (0.1 mg/kg) intravenous bolus injections reduced blood pressure considerably in the L-NAME hypertensive animals. Whole brain NOS activity was reduced by 84%. Hypertension induced by chronic NOS inhibition in LS as well as in RS fed rats seems to be sustained by an interaction of several mechanisms, including the activation of the sympathetic nervous system and the renin-angiotensin system. MESH: Analysis-of-Variance; Antihypertensive-Agents-pharmacology; Arginine-pharmacology; Biphenyl-Compounds-pharmacology; Creatinine-blood; Epinephrine-blood; Heart-Rate-drug-effects; Hypertension-blood; Hypertension-chemically-induced; Imidazoles-pharmacology; Kidney-blood-supply; Kidney-drug-effects; Kidney-pathology; Neuropeptide-Y-blood; Norepinephrine-blood; Phentolamine-pharmacology; Rats-; Rats,-Wistar; Reference-Values; Renin-blood; Renin-Angiotensin-System-drug-effects; Sympathetic-Nervous-System-drug-effects; Tetrazoles-pharmacology; Weight-Gain-drug-effects MESH: *Amino-Acid-Oxidoreductases-antagonists-and-inhibitors; *Arginine-analogs-and-derivatives; *Blood-Pressure-drug-effects; *Brain-enzymology; *Diet,-Sodium-Restricted; *Hypertension-physiopathology; *Renin-Angiotensin-System-physiology; *Sympathetic-Nervous-System-physiology TG: Animal; Comparative-Study; Male PT: JOURNAL-ARTICLE RN: EC 1.14.13.39; EC 1.4.; EC 3.4.23.15; 0; 0; 0; 0; 0; 114798-26-4; 50-60-2; 50903-99-6; 51-41-2; 51-43-4; 60-27-5; 7004-12-8 NM: Nitric-Oxide-Synthase; Amino-Acid-Oxidoreductases; Renin; Antihypertensive-Agents; Biphenyl-Compounds; Imidazoles; Neuropeptide-Y; Tetrazoles; losartan; Phentolamine; NG-Nitroarginine-Methyl-Ester; Norepinephrine; Epinephrine; Creatinine; Arginine AN: 95335885 UD: 9510 -------------------------------------------------------------------------------- Record 17 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Inhibition of basal and reflex-mediated sympathetic activity in the RVLM by nitric oxide. AU: Zanzinger-J; Czachurski-J; Seller-H AD: I. Physiologisches Institut, Universitat Heidelberg, Germany. SO: Am-J-Physiol. 1995 Apr; 268(4 Pt 2): R958-62 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0002-9513 PY: 1995 LA: ENGLISH CP: UNITED-STATES AB: We examined possible functional roles for nitric oxide (NO) in the rostral ventrolateral medulla (RVLM), which is the final area for integration of sympathetic nerve activity (SNA) within the brain stem. Chloralose-anesthetized cats were completely baro- and chemoreceptor denervated, the RVLM was exposed for microinjections, and preganglionic SNA was recorded from the white ramus of the 3rd thoracic segment. Injections of NG-nitro-L-arginine (L-NNA), an inhibitor of NO synthase, but not of NG-nitro-D-arginine, caused distinct increases in SNA and arterial blood pressure (BP). Excitatory somatosympathetic reflex amplitudes evoked by electrical stimulation of the 4th intercostal nerve were significantly increased by L-NNA whereas inhibitory responses to baroreflex activation by stimulation of the carotid sinus nerve were not affected. The effects of L-NNA were counteracted by the NO-donor compounds glyceryltrinitrate and S-nitroso-N-acetylpenicillamine, which decreased BP and SNA below control values at higher doses. These results suggest that endogenous NO, in addition to its peripheral actions, modulates the central nervous control of cardiovascular functions by reduction of basal sympathetic tone and by attenuation of excitatory reflex responses. MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Blood-Pressure-drug-effects; Carotid-Sinus-innervation; Cats-; Electric-Stimulation; Intercostal-Muscles-innervation; Medulla-Oblongata-drug-effects; Nitroglycerin-pharmacology; Penicillamine-analogs-and-derivatives; Penicillamine-pharmacology; Sympathetic-Nervous-System-drug-effects MESH: *Medulla-Oblongata-physiology; *Nitric-Oxide-physiology; *Reflex-physiology; *Sympathetic-Nervous-System-physiology TG: Animal; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 10102-43-9; 2149-70-4; 52-67-5; 55-63-0; 7004-12-8; 79032-48-7 NM: Nitric-Oxide; Nitroarginine; Penicillamine; Nitroglycerin; Arginine; S-nitroso-N-acetylpenicillamine AN: 95251106 UD: 9508 -------------------------------------------------------------------------------- Record 18 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Evidence for a critical role of nitric oxide in the tonic excitation of rabbit renal sympathetic preganglionic neurones. AU: Hakim-MA; Hirooka-Y; Coleman-MJ; Bennett-MR; Dampney-RA AD: Department of Physiology, University of Sydney, NSW, Australia. SO: J-Physiol-Lond. 1995 Jan 15; 482 ( Pt 2): 401-7 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0022-3751 PY: 1995 LA: ENGLISH CP: ENGLAND AB: 1. A large proportion of sympathetic preganglionic neurones contain nitric oxide synthase. The purpose of this study was to determine the effects of facilitation and inhibition of nitric oxide synthesis within the lower thoracic spinal cord (which contains the majority of renal preganglionic neurones) on renal sympathetic nerve activity (rSNA). 2. In anaesthetized rabbits, rSNA was recorded before and after intrathecal injection (50 microliters of 0.5 M solution) of either L-arginine, a precursor of nitric oxide, or N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, into the lower thoracic spinal cord. Spinal cord sections were also stained for the presence of NADPH diaphorase, a marker of nitric oxide synthesizing neurones. 3. A high density of NADPH diaphorase-containing neurones was found within the intermediolateral cell column of the lower thoracic spinal cord. 4. Intrathecal injection of L-arginine and L-NAME resulted in a large increase (113 +/- 25%) and decrease (43 +/- 8%), respectively, in rSNA. In contrast, injection of the inactive isomers D-arginine and D-NAME had no significant effect on rSNA. 5. The results indicate that endogenous nitric oxide in the lower thoracic spinal cord (1) has a potent excitatory action on renal sympathetic preganglionic neurones, and (2) helps to maintain the tonic activity of renal sympathetic nerves under resting conditions. MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; NADPH-Dehydrogenase-analysis; Rabbits-; Spinal-Cord-chemistry; Spinal-Cord-metabolism MESH: *Adrenergic-Fibers-physiology; *Autonomic-Fibers,-Preganglionic-physiology; *Kidney-innervation; *Nitric-Oxide-physiology TG: Animal; Female; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: EC 1.6.99.1; 10102-43-9; 50903-99-6; 7004-12-8 NM: NADPH-Dehydrogenase; Nitric-Oxide; NG-Nitroarginine-Methyl-Ester; Arginine AN: 95230609 UD: 9507 -------------------------------------------------------------------------------- Record 19 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Arterial spontaneous rhythmic contractile activity in humans and rats: spectral analysis and regulatory mechanisms. AU: Rizzoni-D; Castellano-M; Porteri-E; Bettoni-G; Muiesan-P; Muiesan-ML; Giulini-SM; Cinelli-A; Salvetti-M; Agabiti-Rosei-E AD: Chair of Semeiotica e Metodologia Medica, University of Brescia, Italy. SO: J-Hypertens. 1995 Sep; 13(9): 1043-52 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0263-6352 PY: 1995 LA: ENGLISH CP: ENGLAND AB: OBJECTIVE: Many experimental observations have demonstrated the presence of spontaneous cyclic vasomotor activity (CVA) in large and small arteries. This study aimed to evaluate the characteristics of spontaneous CVA in rat and human resistance arteries, and to investigate its possible interference with the evaluation of sympathetic activity by means of spectral analysis of blood pressure in vivo. DESIGN AND RESULTS: In study 1 we examined small mesenteric arteries of spontaneously hypertensive rats and Wistar-Kyoto rats, as well as small omental arteries of normotensive subjects and hypertensive patients (Mulvany and Halpern technique). CVA was enhanced by the agonists of nitric oxide release, and was abolished by the inhibitors of nitric oxide or cyclic GMP synthesis. A potassium channel, which is barium- and zinc-sensitive and tetraethylammonium-insensitive, seems to play a crucial role in the genesis of CVA. In rats and in humans the frequency of CVA fell exactly in the frequency band ('low frequencies') of power spectral analysis of blood pressure usually considered to be an 'index of sympathetic activity'. In study 2, a power spectral analysis of blood pressure variability before and after intra-arterial infusion of noradrenaline or acetylcholine was performed in 18 patients with mild-to-moderate hypertension. The absolute and normalized spectral power of the low-frequency systolic blood pressure peak increased remarkably after noradrenaline and acetylcholine infusion, while its central frequency shifted from 0.10 Hz to approximately 0.06 Hz, exactly the frequency of CVA observed in vitro. CONCLUSIONS: A potassium channel appears to be involved in the genesis of CVA. Also, CVA might contribute to the blood pressure variability independently of the autonomic nervous system activity, and thus probably plays a role in the genesis of the low-frequency peak in the rat and in humans. MESH: Acetylcholine-pharmacology; Adult-; Arteries-drug-effects; Arteries-innervation; Autonomic-Nervous-System-drug-effects; Blood-Pressure-drug-effects; Heart-Rate-drug-effects; Middle-Age; Norepinephrine-pharmacology; Rats-; Rats,-Inbred-SHR; Rats,-Inbred-WKY; Spectrum-Analysis; Sympathomimetics-pharmacology; Vasomotor-System-drug-effects MESH: *Arteries-physiopathology; *Hypertension-physiopathology; *Vasomotor-System-physiology TG: Animal; Female; Human; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 0; 51-41-2; 51-84-3 NM: Sympathomimetics; Norepinephrine; Acetylcholine AN: 96155746 UD: 9605 -------------------------------------------------------------------------------- Record 20 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Nitric oxide synthase-containing neurons in rat parasympathetic, sympathetic and sensory ganglia: a comparative study. AU: Alm-P; Uvelius-B; Ekstrom-J; Holmqvist-B; Larsson-B; Andersson-KE AD: Department of Pathology, University of Lund, Lund University Hospital, Sweden. SO: Histochem-J. 1995 Oct; 27(10): 819-31 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0018-2214 PY: 1995 LA: ENGLISH CP: ENGLAND AB: In rats, the distribution of nerve structures staining for NADPH-diaphorase, and showing immunoreactivities for nitric oxide synthase (NOS), tyrosine hydroxylase and various neuropeptides was studied in sensory ganglia (dorsal root, nodose and trigeminal ganglia), in sympathetic ganglia (superior cervical, stellate, coeliac-superior and inferior mesenteric ganglia), parasympathetic ganglia (sphenopalatine, submandibular, sublingual and otic ganglia), and in the mixed parasympathetic/sympathetic ganglia (major pelvic ganglia). The coincidence of neuronal cell bodies with strong NOS-immunoreactivity and strong NADPH diaphorase reactivity was almost total. The relative proportions of NOS-immunoreactive nerve cell bodies were largest in parasympathetic ganglia and major pelvic ganglia followed by sensory ganglia. In sympathetic ganglia no NOS-immunoreactive neuronal cell bodies could be detected. In parasympathetic and major pelvic ganglia, there was a very significant neuronal co-localization of immunoreactivities for NOS and vasoactive intestinal polypeptide (VIP). This was almost total in major pelvic ganglia, in which NOS-/VIP-immunoreactive nerve cell bodies were separate from sympathetic (tyrosine hydroxylase-/neuropeptide Y-immunoreactive), suggesting that NOS-/VIP-immuno-reactive neurons might also be parasympathetic. MESH: Ganglia,-Parasympathetic-ultrastructure; Ganglia,-Sensory-ultrastructure; Ganglia,-Sympathetic-ultrastructure; Immunohistochemistry-; Nerve-Fibers-enzymology; Neurons-ultrastructure; Neuropeptides-analysis; NADPH-Dehydrogenase-metabolism; Rats-; Tyrosine-3-Monooxygenase-analysis MESH: *Ganglia,-Parasympathetic-enzymology; *Ganglia,-Sensory-enzymology; *Ganglia,-Sympathetic-enzymology; *Neurons-enzymology; *Nitric-Oxide-Synthase-analysis TG: Animal; Comparative-Study; Female; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: EC 1.14.13.39; EC 1.14.16.2; EC 1.6.99.1; 0 NM: Nitric-Oxide-Synthase; Tyrosine-3-Monooxygenase; NADPH-Dehydrogenase; Neuropeptides AN: 96162427 UD: 9605 -------------------------------------------------------------------------------- Record 21 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Histochemistry of nitric oxide synthase in the nervous system. AU: Blottner-D; Grozdanovic-Z; Gossrau-R AD: Department of Anatomy, Free University of Berlin, Germany. SO: Histochem-J. 1995 Oct; 27(10): 785-811 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0018-2214 PY: 1995 LA: ENGLISH CP: ENGLAND AB: Nitric oxide synthase, which generates the physiological messenger molecule nitric oxide, and its associated NADPH diaphorase (NADPHd) activity are distributed throughout selective neuronal populations of the central and peripheral nervous system. Considerable evidence has been accumulated to indicate that NADPHd activity labels cells lacking neuronal nitric oxide synthase, i.e., the specificity of the reaction has to be considered for the reliable detection of the enzyme in neuronal but also non-neuronal tissue. In the present review, critical aspects of nitric oxide synthase visualization in neurones, using its NADPHd activity, are discussed. Furthermore, the organization of the central and peripheral nitric oxide synthase-containing neuronal systems is described. Nitric oxide synthase is present in local cortical and striatal neurones, hypothalamic magnocellular neurones, mesopontine cholinergic neurones, cerebellar interneurones, preganglionic sympathetic and parasympathetic neurones, neurones in parasympathetic autonomic and enteric ganglia and primary viscero-afferent neurones. Finally, injury-related alterations in nitric oxide synthase activity are briefly outlined. In this respect, the histochemistry of nitric oxide synthase may represent a valuable marker for neurochemical, if not structural, alterations observed in neural diseases, regeneration and transplantation. MESH: Neurons-enzymology; NADPH-Dehydrogenase-metabolism MESH: *Histocytochemistry-; *Nervous-System-enzymology; *Nitric-Oxide-Synthase-metabolism TG: Animal; Human PT: JOURNAL-ARTICLE; REVIEW; REVIEW,-ACADEMIC RN: EC 1.14.13.39; EC 1.6.99.1 NM: Nitric-Oxide-Synthase; NADPH-Dehydrogenase AN: 96162425 UD: 9605 -------------------------------------------------------------------------------- Record 22 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: A new perspective on the inhibitory role of nitric oxide in sympathetic neurotransmission. AU: Macarthur-H; Mattammal-MB; Westfall-TC AD: Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, Missouri, USA. SO: Biochem-Biophys-Res-Commun. 1995 Nov 13; 216(2): 686-92 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0006-291X PY: 1995 LA: ENGLISH CP: UNITED-STATES AB: By using, as a model of sympathetic neurons, immortalized rat pheochromocytoma (PC12) cells differentiated by nerve growth factor (NGF), the effect of nitric oxide on sympathetic neurotransmission was examined. The NO donor sodium nitroprusside (SNP; 10(-4)-3 x 10(-4) M) caused an apparent inhibition of dopamine release from PC12 cells, as measured by HPLC. Studies, in the absence of cells, involving the incubation of dopamine (20 ng/ml) or norepinephrine (15 ng/ml) with SNP (10(-6)-3 x 10(-4) M) or authentic NO (6 x 10(-6)-3 x 10(-5) M) revealed a similar reduction in the detection of the catecholamines. In addition, absorption spectroscopy studies showed dopamine and norepinephrine to be oxidized by NO resulting in the formation of their respective quinone products. These observations, coupled with the finding that the ability of dopamine to raise cAMP levels within PC12 cells was reduced after incubation with SNP, reveal that NO inhibits the biological activity rather than the release of catecholamines. MESH: Adrenal-Gland-Neoplasms; Cell-Differentiation-drug-effects; Cyclic-AMP-metabolism; Dopamine-metabolism; Dopamine-pharmacology; Dose-Response-Relationship,-Drug; Drug-Interactions; Kinetics-; Nerve-Growth-Factors-pharmacology; Neurons-cytology; Neurons-drug-effects; Norepinephrine-metabolism; Norepinephrine-pharmacology; Pheochromocytoma-; PC12-Cells; Rats-; Synaptic-Transmission-drug-effects MESH: *Neurons-physiology; *Nitric-Oxide-pharmacology; *Nitric-Oxide-physiology; *Nitroprusside-pharmacology; *Sympathetic-Nervous-System-physiology; *Synaptic-Transmission-physiology TG: Animal; Comparative-Study; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: HL226319HLNHLBI; HL35202HLNHLBI RN: 0; 10102-43-9; 15078-28-1; 51-41-2; 51-61-6; 60-92-4 NM: Nerve-Growth-Factors; Nitric-Oxide; Nitroprusside; Norepinephrine; Dopamine; Cyclic-AMP AN: 96063662 UD: 9602 -------------------------------------------------------------------------------- Record 23 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Role of nitric oxide in regulation of baroreceptor reflex. AU: Jimbo-M; Suzuki-H; Ichikawa-M; Kumagai-K; Nishizawa-M; Saruta-T AD: Department of Internal Medicine, School of Medicine Keio University, Tokyo, Japan. SO: J-Auton-Nerv-Syst. 1994 Dec 15; 50(2): 209-19 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0165-1838 PY: 1994 LA: ENGLISH CP: NETHERLANDS AB: The possible role of nitric oxide (NO) on modulating sympathetic nerve activity through its action on baroreceptor reflex arc was investigated. L-Arginine, a precursor of NO, and NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, were separately infused intravenously in increasing doses in 126 pentobarbital-anesthetized rabbits. Mean arterial pressure (MAP), heart rate (HR), aortic nerve activity (ANA), cervical (CSNA) and renal sympathetic nerve activities (RSNA) were recorded. L-Arginine infusion decreased MAP (P < 0.05), ANA (P < 0.05), CSNA (P < 0.05) and RSNA (P < 0.05) without changes in HR. Infusion of D-arginine, an enantiomer of L-arginine, and simultaneous infusion of L-arginine and L-NMMA, did not elicit such changes. L-NMMA infusion increased MAP (P < 0.05) and ANA (P < 0.05) and decreased HR (P < 0.05), while it tended to increase CSNA and RSNA without significance. Infusion of L-arginine or L-NMMA did not alter the slope of ANA, CSNA, RSNA, or HR in relation to MAP. These results suggest that NO modulates efferent sympathetic nerve activity, not by altering the afferent or efferent limbs of the baroreceptor reflex arc, but by interacting with the sympathetic pathway in the central nervous system. MESH: Afferent-Pathways-cytology; Afferent-Pathways-drug-effects; Afferent-Pathways-physiology; Amino-Acid-Oxidoreductases-antagonists-and-inhibitors; Aorta-innervation; Aorta-physiology; Arginine-analogs-and-derivatives; Arginine-pharmacology; Baroreflex-drug-effects; Blood-Pressure-drug-effects; Blood-Pressure-physiology; Heart-Rate-drug-effects; Heart-Rate-physiology; Kidney-innervation; Kidney-physiology; Nitric-Oxide-antagonists-and-inhibitors; Nitroglycerin-pharmacology; Rabbits-; Receptors,-Presynaptic-drug-effects; Receptors,-Presynaptic-physiology; Sympathetic-Nervous-System-cytology; Sympathetic-Nervous-System-drug-effects; Sympathetic-Nervous-System-physiology MESH: *Baroreflex-physiology; *Nitric-Oxide-physiology TG: Animal; Female; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: EC 1.14.13.39; EC 1.4.; 0; 10102-43-9; 17035-90-4; 55-63-0; 7004-12-8 NM: Nitric-Oxide-Synthase; Amino-Acid-Oxidoreductases; Receptors,-Presynaptic; Nitric-Oxide; omega-N-Methylarginine; Nitroglycerin; Arginine AN: 95190226 UD: 9506 -------------------------------------------------------------------------------- Record 24 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Nitric oxide suppression of norepinephrine release from nerves in the superior mesenteric artery. AU: Macedo-MP; Lautt-WW AD: Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Canada. SO: Proc-West-Pharmacol-Soc. 1994; 37: 103-4 ISSN: 0083-8969 PY: 1994 LA: ENGLISH CP: UNITED-STATES MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Blood-Pressure-drug-effects; Cats-; Mesenteric-Artery,-Superior-drug-effects; Muscle,-Smooth,-Vascular-drug-effects; Nitric-Oxide-antagonists-and-inhibitors; Sympathetic-Nervous-System-drug-effects MESH: *Mesenteric-Artery,-Superior-innervation; *Mesenteric-Artery,-Superior-metabolism; *Muscle,-Smooth,-Vascular-innervation; *Muscle,-Smooth,-Vascular-metabolism; *Nitric-Oxide-pharmacology; *Norepinephrine-metabolism TG: Animal; Female; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 10102-43-9; 50903-99-6; 51-41-2; 7004-12-8 NM: Nitric-Oxide; NG-Nitroarginine-Methyl-Ester; Norepinephrine; Arginine AN: 95075879 UD: 9503 -------------------------------------------------------------------------------- Record 25 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Inhibition of sympathetic vasoconstriction is a major principle of vasodilation by nitric oxide in vivo. AU: Zanzinger-J; Czachurski-J; Seller-H AD: I. Physiologisches Institut, Universitat Heidelberg, Germany. SO: Circ-Res. 1994 Dec; 75(6): 1073-7 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0009-7330 PY: 1994 LA: ENGLISH CP: UNITED-STATES AB: The objective of this study was to determine whether vasodilator effects of nitric oxide (NO) can be explained by the inhibition of vasoconstriction caused by peripheral sympathetic nerve activity (SNA) in vivo. For this purpose, we studied the effects of systemic inhibition of NO synthesis during experimental variation of SNA in anesthetized cats. Intravenous infusion of NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg) in baroreceptor-intact animals (n = 6) caused increases in mean arterial blood pressure (MAP) from 105.8 +/- 3.4 to 192.0 +/- 4.3 mm Hg that were associated with slight decreases in preganglionic SNA recorded from the white ramus of the third thoracic segment. Higher SNA appeared in completely baroreceptor-denervated cats (n = 10) than in the intact cats, but no changes in nerve activity occurred after the subsequent administration of L-NAME. In contrast, MAP increased from 123.3 +/- 4.0 to 245.8 +/- 5.1 mm Hg. In baroreceptor-denervated cats, reversible suppression of peripheral SNA produced by cooling of the ventral surface of the rostral ventrolateral medulla oblongata (RVLM) caused significant hypotension (61.1 +/- 2.6 mm Hg) and almost completely reversed the hypertension caused by L-NAME (76.0 +/- 3.7 mm Hg). Intravenous administration of the alpha 1-adrenergic receptor antagonist prazosin after L-NAME reduced MAP to a similar extent. In contrast, hypertension induced by angiotensin II could not be reversed by RVLM cooling. The pressor effects of intravenously administered noradrenaline during RVLM cooling were markedly potentiated by L-NAME and attenuated by the NO-donor compound S-nitroso-N-acetylpenicillamine (SNAP).(ABSTRACT TRUNCATED AT 250 WORDS) MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Blood-Pressure-drug-effects; Cats-; Dose-Response-Relationship,-Drug; Infusions,-Intravenous; Nitric-Oxide-antagonists-and-inhibitors; Nitric-Oxide-biosynthesis; Norepinephrine-administration-and-dosage; Norepinephrine-pharmacology; Penicillamine-analogs-and-derivatives; Penicillamine-pharmacology; Sympathetic-Nervous-System-drug-effects; Vasoconstriction-drug-effects MESH: *Nitric-Oxide-physiology; *Sympathetic-Nervous-System-physiology; *Vasoconstriction-physiology; *Vasodilation-drug-effects; *Vasodilation-physiology TG: Animal; Comparative-Study; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 10102-43-9; 50903-99-6; 51-41-2; 52-67-5; 7004-12-8; 79032-48-7 NM: Nitric-Oxide; NG-Nitroarginine-Methyl-Ester; Norepinephrine; Penicillamine; Arginine; S-nitroso-N-acetylpenicillamine AN: 95043134 UD: 9502 -------------------------------------------------------------------------------- Record 26 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Inhibition of nitric oxide synthesis augments centrally induced sympathetic coronary vasoconstriction in cats. AU: Goodson-AR; Leibold-JM; Gutterman-DD AD: Veterans Administration Medical Center, Iowa City, Iowa. SO: Am-J-Physiol. 1994 Oct; 267(4 Pt 2): H1272-8 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0002-9513 PY: 1994 LA: ENGLISH CP: UNITED-STATES AB: The principal effect of sympathetic activation on the coronary circulation is an alpha-adrenergic coronary vasoconstriction in the presence of beta-receptor blockade. Secondary effects include vasodilation due to beta-adrenoceptor stimulation and alpha 2-mediated release of endothelium-derived relaxing factor (EDRF) from the coronary vascular endothelium. We hypothesized that blockade of nitric oxide synthesis (nitro-L-arginine methyl ester, L-NAME) would augment coronary vasoconstriction to sympathetic stimulation as a result of a decrease in alpha 2-mediated EDRF release. In chloralose-anesthetized cats, hypothalamic stimulation produced increases in coronary vascular resistance [maximum 26 +/- 9% (SE)] and arterial pressure (41 +/- 7%) and a decrease in coronary blood flow velocity (15 +/- 6%). L-NAME (3 mg/kg iv) increased baseline arterial pressure from 69 +/- to 92 +/- 7 mmHg (P < 0.05). After L-NAME, a greater increase in coronary vascular resistance (55 +/- 20%, P < 0.05), a decrease in coronary blood flow velocity (24 +/- 7%, P < 0.05), and a similar pressor response (34 +/- 7%) were observed in response to hypothalamic stimulation. L-Arginine reversed the effect of L-NAME on coronary vasoconstriction to hypothalamic stimulation. Similar increases in arterial pressure (from 73 +/- 3 to 91 +/- 5 mmHg, P < 0.05) with vasopressin (0.01-0.05 U/min) failed to enhance coronary vasoconstriction to activation in anterior hypothalamus. We conclude that inhibition of EDRF synthesis augments centrally induced sympathetic coronary vasoconstriction in the cat. MESH: Arginine-pharmacology; Blood-Flow-Velocity-drug-effects; Blood-Pressure-drug-effects; Blood-Pressure-physiology; Cats-; Coronary-Vessels-drug-effects; Coronary-Vessels-innervation; Electric-Stimulation; Endothelium-Derived-Relaxing-Factor-secretion; Hypothalamus-drug-effects; Muscle,-Smooth,-Vascular-drug-effects; Muscle,-Smooth,-Vascular-innervation; Nitric-Oxide-antagonists-and-inhibitors; Sympathetic-Nervous-System-drug-effects; Time-Factors; Vascular-Resistance-drug-effects; Vascular-Resistance-physiology; Vasodilation-drug-effects; Vena-Cava,-Inferior-physiology MESH: *Arginine-analogs-and-derivatives; *Coronary-Vessels-physiology; *Hypothalamus-physiology; *Muscle,-Smooth,-Vascular-physiology; *Nitric-Oxide-biosynthesis; *Sympathetic-Nervous-System-physiology; *Vasoconstriction-drug-effects; *Vasopressins-pharmacology TG: Animal; Female; Male; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-Non-P.H.S.; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: HL032295HLNHLBI RN: 0; 0; 10102-43-9; 50903-99-6; 7004-12-8 NM: Endothelium-Derived-Relaxing-Factor; Vasopressins; Nitric-Oxide; NG-Nitroarginine-Methyl-Ester; Arginine AN: 95029944 UD: 9501 -------------------------------------------------------------------------------- Record 27 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Is nitric oxide involved in the tonic inhibition of central sympathetic outflow in humans? AU: Hansen-J; Jacobsen-TN; Victor-RG AD: Department of Internal Medicine, UT Southwestern Medical Center, Dallas 75235-8573. SO: Hypertension. 1994 Oct; 24(4): 439-44 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0194-911X PY: 1994 LA: ENGLISH CP: UNITED-STATES AB: Recent studies in experimental animals have advanced the concept that neuronal nitric oxide is an important component of the signal transduction pathways that tonically restrain sympathetic vasoconstrictor outflow from the brain stem. To determine whether or not this concept can be extended to the control of sympathetic outflow in humans, we recorded muscle sympathetic nerve activity (microelectrodes, peroneal nerve) in healthy human subjects during intravenous infusion of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) (3.6 to 6.7 mg/kg). The major new finding is that during intravenous L-NMMA mean arterial pressure increased (10 +/- 2 mm Hg, P < .05), whereas heart rate and sympathetic nerve activity decreased (P < .05) by 10 +/- 2 beats per minute and 61 +/- 5%, respectively. These reflex decreases were indistinguishable from those produced when blood pressure was increased comparably with phenylephrine, an internal vasoconstrictor control. When the L-NMMA-induced increase in blood pressure was attenuated experimentally to minimize baroreflex activation, sympathetic nerve activity and heart rate were unchanged. Furthermore, during infusion of L-arginine (323 to 513 mg/kg IV) to increase nitric oxide synthesis, mean arterial pressure decreased (12 +/- 2 mm Hg, P < .05), but heart rate and sympathetic nerve activity increased (P < .05) by 11 +/- 2 beats per minute and 98 +/- 27%, respectively. Thus, our experiments in humans provide no support for the emerging concept that nitric oxide is involved in the tonic restraint of central sympathetic outflow. MESH: Adult-; Arginine-administration-and-dosage; Arginine-pharmacology; Blood-Pressure-drug-effects; Heart-Rate-drug-effects; Infusions,-Intravenous; Microelectrodes-; Muscles-drug-effects; Nitric-Oxide-physiology; Peroneal-Nerve-physiology; Phenylephrine-administration-and-dosage; Phenylephrine-pharmacology MESH: *Arginine-analogs-and-derivatives; *Endothelium-Derived-Relaxing-Factor-antagonists-and-inhibitors; *Nitric-Oxide-antagonists-and-inhibitors; *Sympathetic-Nervous-System-drug-effects TG: Human; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: 1F05TW0494901TWFIC; 1F05TW0449401TWFIC RN: 0; 10102-43-9; 17035-90-4; 59-42-7; 7004-12-8 NM: Endothelium-Derived-Relaxing-Factor; Nitric-Oxide; omega-N-Methylarginine; Phenylephrine; Arginine AN: 94375158 UD: 9412 -------------------------------------------------------------------------------- Record 28 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Nitric oxide increases renal blood flow by interacting with the sympathetic nervous system. AU: Kumagai-K; Suzuki-H; Ichikawa-M; Jimbo-M; Murakami-M; Ryuzaki-M; Saruta-T AD: Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan. SO: Hypertension. 1994 Aug; 24(2): 220-6 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0194-911X PY: 1994 LA: ENGLISH CP: UNITED-STATES AB: To investigate whether changes in renal blood flow induced by nondepressor doses of L-arginine, the precursor of nitric oxide, are mediated by a sympathetic neural mechanism, we examined the following in conscious rabbits: (1) the effects of intravenous infusion of L- or D-arginine (15 to 200 mumol/kg per minute) on renal blood flow and renal sympathetic nerve activity with or without intravenous infusion of a nonpressor dose of NG-monomethyl-L-arginine (L-NMMA), a nitric oxide synthase inhibitor, and (2) the effects of L-arginine on renal blood flow after renal denervation with or without L-NMMA pretreatment. In renal innervated rabbits, L-arginine (100 and 200 mumol/kg per minute) increased renal blood flow by 9 +/- 2 and 16 +/- 3 mL/min (P < .05, respectively) and decreased renal sympathetic nerve activity by 12 +/- 4% and 19 +/- 3% of control (P < .05, respectively). In contrast, no changes occurred in any variable during D-arginine infusion. L-NMMA attenuated the renal blood flow and renal sympathetic nerve activity responses to L-arginine (P < .05). In renal denervated rabbits, L-NMMA also attenuated the renal blood flow responses to L-arginine (P < .05) and abolished them (P < .05) compared with those in renal innervated rabbits. All renal blood flow responses to L-arginine were accompanied by parallel changes in plasma L-citrulline concentration.(ABSTRACT TRUNCATED AT 250 WORDS) MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Citrulline-blood; Rabbits-; Sympathetic-Nervous-System-drug-effects MESH: *Kidney-innervation; *Nitric-Oxide-physiology; *Renal-Circulation; *Sympathetic-Nervous-System-physiology TG: Animal; Female; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 10102-43-9; 17035-90-4; 372-75-8; 7004-12-8 NM: Nitric-Oxide; omega-N-Methylarginine; Citrulline; Arginine AN: 94314389 UD: 9410 -------------------------------------------------------------------------------- Record 29 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Modulation by the endothelium of sympathetic vasoconstriction in an in vitro preparation of the rat tail artery. AU: Thorin-E; Atkinson-J AD: Laboratoire de Pharmacologie cardio-vasculaire, Faculte des Sciences Pharmaceutiques et Biologiques, Nancy, France. SO: Br-J-Pharmacol. 1994 Jan; 111(1): 351-7 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0007-1188 PY: 1994 LA: ENGLISH CP: ENGLAND AB: 1. The influence of the endothelium on transmural electrical stimulation was investigated in isolated and perfused segments of the rat tail artery. Noradrenaline release (NA, quantified by h.p.l.c.-electrochemical detection) and changes in perfusion pressure (PP, measured at constant flow rate) were simultaneously recorded in unstimulated and stimulated arterial segments, in the absence and in the presence of drugs. The ratio PP/NA release (mmHg pg-1) was taken as an index of the noradrenergic effectiveness. 2. Removal of the endothelium produced an increase in NA release and PP, in unstimulated and stimulated arteries. This can be taken as evidence of an endothelium-derived inhibitory factor (EDIF) acting at the prejunctional level, inhibiting NA release. Furthermore, in unstimulated arteries, the ratio PP/NA release decreased suggesting the existence of an endothelium-derived contracting factor (EDCF). 3. Perfusion of arteries with N omega-nitro-L-arginine methyl ester (L-NAME, 10 microM) or methylene blue (MeB, 0.5 microM) had no effect on PP or NA release in unstimulated arteries. In stimulated arteries, both drugs potentiated the increase in PP without changing NA release and therefore, led to an increase in noradrenergic effectiveness. After removal of the endothelium, neither L-NAME nor MeB affected the increases in PP and NA release following electrical stimulation. 4. Carbachol (1 microM) attenuated both NA release and the increase in PP during electrical stimulation, and increased the ratio PP/NA release. L-NAME and MeB did not modify the inhibitory effect of carbachol on NA release, or the facilitatory effect of carbachol on the noradrenergic effectiveness.(ABSTRACT TRUNCATED AT 250 WORDS) MESH: Angiotensin-II-pharmacology; Arginine-analogs-and-derivatives; Arginine-pharmacology; Arteries-drug-effects; Arteries-metabolism; Arteries-physiology; Carbachol-pharmacology; Electric-Stimulation; Endothelium,-Vascular-cytology; Endothelium,-Vascular-drug-effects; Methylene-Blue-pharmacology; Muscle-Contraction-drug-effects; Muscle,-Smooth,-Vascular-physiology; Nitric-Oxide-antagonists-and-inhibitors; Norepinephrine-pharmacology; Rats-; Rats,-Wistar; Tail-blood-supply MESH: *Endothelium,-Vascular-physiology; *Muscle,-Smooth,-Vascular-drug-effects; *Norepinephrine-metabolism; *Sympathetic-Nervous-System-physiology; *Vasoconstriction-drug-effects TG: Animal; In-Vitro; Male PT: JOURNAL-ARTICLE RN: 10102-43-9; 11128-99-7; 50903-99-6; 51-41-2; 51-83-2; 61-73-4; 7004-12-8 NM: Nitric-Oxide; Angiotensin-II; NG-Nitroarginine-Methyl-Ester; Norepinephrine; Carbachol; Methylene-Blue; Arginine AN: 94282475 UD: 9409 -------------------------------------------------------------------------------- Record 30 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Sympathetic baroreceptor responses after chronic NG-nitro-L-arginine methyl ester treatment in conscious rats. AU: Scrogin-KE; Veelken-R; Luft-FC AD: Franz Volhard Clinic, Rudolf Virchow University Hospitals, Free University of Berlin, FRG. SO: Hypertension. 1994 Jun; 23(6 Pt 2): 982-6 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0194-911X PY: 1994 LA: ENGLISH CP: UNITED-STATES AB: Blood pressure elevations after nitric oxide inhibition may result in part from increased sympathetic tone. In this study arterial baroreceptor reflex control of heart rate, renal sympathetic nerve activity (RSNA), and adrenal sympathetic nerve activity (ASNA) were compared in rats given normal tap water or a 3.7 nmol/L (10 mg%) solution of NG-nitro-L-arginine methyl ester (L-NAME) for 1 or 5 weeks. L-NAME raised blood pressure after 5 weeks of treatment (153 +/- 3 versus 130 +/- 3 and 124 +/- 2 mm Hg, 5 weeks versus 1 week and control). The sensitivity of arterial baroreceptor reflex control of RSNA was reduced after both 1 and 5 weeks of treatment (-5.05 +/- 0.63% and -4.46 +/- 0.2% versus -6.43 +/- 0.39% baseline activity per millimeters of mercury). Set point gain of ASNA was attenuated after 5 weeks of treatment compared with controls (-1.7 +/- 3% versus -3.3 +/- 3% baseline activity per millimeters of mercury). Maximal inhibition of ASNA was attenuated in groups treated 1 and 5 weeks (60 +/- 3% and 66 +/- 3% versus 34 +/- 4% baseline activity). The maximal increase in both RSNA and ASNA was elevated in rats treated 5 weeks (RSNA: control, 263 +/- 19%; 1 week, 224 +/- 17%; 5 weeks, 324 +/- 20%; ASNA: control, 272 +/- 29%; 1 week, 252 +/- 31%; 5 weeks, 361 +/- 28% baseline activity). The data indicate that chronic L-NAME treatment alters arterial baroreceptor reflexes in part before the onset of hypertension. MESH: Adrenal-Glands-innervation; Arginine-pharmacology; Arteries-innervation; Baroreflex-physiology; Blood-Pressure-drug-effects; Kidney-innervation; Nitric-Oxide-antagonists-and-inhibitors; Rats-; Rats,-Sprague-Dawley; Sympathetic-Nervous-System-physiology; Time-Factors MESH: *Arginine-analogs-and-derivatives; *Baroreflex-drug-effects; *Sympathetic-Nervous-System-drug-effects TG: Animal; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 10102-43-9; 50903-99-6; 7004-12-8 NM: Nitric-Oxide; NG-Nitroarginine-Methyl-Ester; Arginine AN: 94266464 UD: 9409 -------------------------------------------------------------------------------- Record 31 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Hypertension induced by nitric oxide synthesis inhibition is renal nerve dependent. AU: Matsuoka-H; Nishida-H; Nomura-G; Van-Vliet-BN; Toshima-H AD: Third Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan. SO: Hypertension. 1994 Jun; 23(6 Pt 2): 971-5 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0194-911X PY: 1994 LA: ENGLISH CP: UNITED-STATES AB: Recent studies have indicated that chronic administration of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, produces marked hypertension. Although the mechanism of this form of hypertension is not well understood, several studies have demonstrated that sympathetic nerve activity is at least acutely elevated after L-NAME administration. To evaluate the potential role of the renal sympathetic nerves in L-NAME-induced hypertension, we compared the blood pressure response to L-NAME in four groups of Sprague-Dawley rats (n = 8 each): (1) sham-operated vehicle-treated, (2) sham-operated L-NAME-treated, (3) denervated vehicle-treated, and (4) denervated L-NAME-treated. After renal denervation or sham surgery, L-NAME was added to the drinking water (70 mg/100 mL) for 4 weeks, and arterial pressure was measured weekly by the tail-cuff method. L-NAME treatment caused a progressive increase in arterial pressure in sham-operated rats, rising to 154 +/- 6 mm Hg by week 4 of treatment compared with 115 +/- 2 mm Hg in the vehicle-treated sham-operated group (P < .005). In contrast, the development of hypertension was significantly delayed and attenuated in renal-denervated rats treated with L-NAME. The results of our study suggest that L-NAME-induced hypertension may be partly mediated by or is at least dependent on the integrity of the renal nerves. MESH: Arginine-pharmacology; Blood-Pressure-drug-effects; Denervation-; Kidney-metabolism; Norepinephrine-metabolism; Rats-; Rats,-Sprague-Dawley; Renin-blood MESH: *Arginine-analogs-and-derivatives; *Hypertension-chemically-induced; *Kidney-innervation; *Nitric-Oxide-antagonists-and-inhibitors; *Sympathetic-Nervous-System-physiology TG: Animal; Comparative-Study; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: EC 3.4.23.15; 10102-43-9; 50903-99-6; 51-41-2; 7004-12-8 NM: Renin; Nitric-Oxide; NG-Nitroarginine-Methyl-Ester; Norepinephrine; Arginine AN: 94266462 UD: 9409 -------------------------------------------------------------------------------- Record 32 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: The effects of NG-nitro-L-arginine, a nitric oxide synthase inhibitor, on norepinephrine overflow and antidiuresis induced by stimulation of renal nerves in anesthetized dogs. AU: Egi-Y; Matsumura-Y; Murata-S; Umekawa-T; Hisaki-K; Takaoka-M; Morimoto-S AD: Department of Pharmacology, Osaka University of Pharmaceutical Sciences, Japan. SO: J-Pharmacol-Exp-Ther. 1994 May; 269(2): 529-35 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0022-3565 PY: 1994 LA: ENGLISH CP: UNITED-STATES AB: We examined the involvement of endogenous nitric oxide (NO) in noradrenergic neurotransmission and renal function in anesthetized dogs, by using NG-nitro-L-arginine (NOARG), a NO synthase inhibitor. Renal nerve stimulation (RNS) produced the frequency-dependent increase in the rate of norepinephrine secretion. The low frequency RNS (0.5-2.0 Hz) decreased urine flow and urinary excretion of sodium, without affecting renal hemodynamics. High frequency RNS (2.5-5.0 Hz) caused a more potent antidiuresis and renal vasoconstriction that resulted in reductions in renal blood flow and glomerular filtration rate. Intrarenal arterial infusion of NOARG, at a dose (10 micrograms/kg/min) which had no effect on renal hemodynamics, significantly enhanced the RNS-induced reductions of urine formation and renal vasoconstriction and increments in norepinephrine secretion rate. Qualitatively similar results were observed with a higher dose of NOARG (40 micrograms/kg/min), although this dose did decrease basal levels of renal blood flow and urine flow. Enhancement of NOARG on RNS-induced actions was abolished by the simultaneous administration of L-arginine. Endogenous NO probably has a role as inhibitory modulator of renal noradrenergic neurotransmission. MESH: Arginine-pharmacology; Dogs-; Electric-Stimulation; Kidney-blood-supply; Kidney-drug-effects; Kidney-innervation; Nitric-Oxide-antagonists-and-inhibitors; Sympathetic-Nervous-System-drug-effects; Sympathetic-Nervous-System-physiology; Vasoconstriction-drug-effects MESH: *Amino-Acid-Oxidoreductases-antagonists-and-inhibitors; *Arginine-analogs-and-derivatives; *Diuresis-drug-effects; *Kidney-physiology; *Nitric-Oxide-physiology; *Norepinephrine-metabolism TG: Animal; Female; Male PT: JOURNAL-ARTICLE RN: EC 1.14.13.39; EC 1.4.; 10102-43-9; 17035-90-4; 51-41-2; 7004-12-8 NM: Nitric-Oxide-Synthase; Amino-Acid-Oxidoreductases; Nitric-Oxide; omega-N-Methylarginine; Norepinephrine; Arginine AN: 94238441 UD: 9408 -------------------------------------------------------------------------------- Record 33 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Endogenous nitric oxide modulates vasopressor responses, but not depressor responses, to spinal sympathetic nerve stimulation in pithed rats. AU: MacLean-MR; Graham-J; McGrath-JC AD: Autonomic Physiology Unit, Glasgow University, Scotland. SO: J-Cardiovasc-Pharmacol. 1994 Feb; 23(2): 319-25 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0160-2446 PY: 1994 LA: ENGLISH CP: UNITED-STATES AB: The effects of N omega-nitro-L-arginine methylester (L-NAME), an inhibitor of nitric oxide (NO) synthase (1,5, and 10 mg/kg) on vasopressor and depressor responses to segmental sympathetic nerve stimulation were studied in the pithed rat preparation. Vasopressor responses were evoked by stimulation of the spinal sympathetic outflow at T6-T8 (30 V, 0.05 ms at 5 Hz with 10 pulses). This pressor response was biphasic: An initial transient response (to nerve stimulation) was followed by a later prolonged response (to adrenal catecholamine release). L-NAME 1, 5, and 10 mg/kg increased mean arterial blood pressure (MAP); this effect was maximal at 1 mg/kg L-NAME, but had no effect on heart rate (HR). L-NAME 1, 5, and 10 mg/kg potentiated both phases of the pressor response; the effect was maximal at 10 mg/kg. Vasodepressor responses were evoked by stimulation of the spinal sympathetic outflow at S2-L6 (30 V, 0.05 ms at 5 Hz with 10 pulses). L-NAME 1, 5, and 10 mg/kg did not inhibit these depressor responses. We conclude that inhibition of the synthesis of endogenous NO causes a hypertension in pithed rats that is associated with increased vasoconstriction in response to sympathetic nerve stimulation and adrenal catecholamine release. Systemic vascular depressor responses to segmental sympathetic nerve stimulation are not affected, however; therefore, NO cannot be the major mediator of these responses. MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Blood-Pressure-drug-effects; Electric-Stimulation; Endothelins-pharmacology; Heart-Rate-drug-effects; Nitric-Oxide-antagonists-and-inhibitors; Rats-; Rats,-Wistar MESH: *Blood-Pressure-physiology; *Decerebrate-State-physiopathology; *Nitric-Oxide-physiology; *Spinal-Cord-physiology; *Sympathetic-Nervous-System-physiology TG: Animal; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 0; 10102-43-9; 50903-99-6; 7004-12-8 NM: Endothelins; Nitric-Oxide; NG-Nitroarginine-Methyl-Ester; Arginine AN: 94194954 UD: 9407 -------------------------------------------------------------------------------- Record 34 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Nitric oxide modulates sympathetic neurotransmission at the prejunctional level. AU: Addicks-K; Bloch-W; Feelisch-M AD: Department of Anatomy, University of Cologne, Germany. SO: Microsc-Res-Tech. 1994 Oct 1; 29(2): 161-8 ISSN: 1059-910X PY: 1994 LA: ENGLISH CP: UNITED-STATES AB: In spite of accumulating evidence for a modulation of sympathetic neurotransmission by endogenously produced nitric oxide (NO), it remains unclear in which parts of the vascular system and at what level this interaction takes place. The aim of the present study was to investigate the distribution of endothelial and neuronal NO synthase (NOS) along the vascular tree of the heart at the light and electron microscopic level using NADPH-diaphorase (NADPH-d) staining as a marker for NOS. In addition, the functional effects of exogenous NO on coronary vascular resistance and cardiac adrenergic nerves was studied using the isolated perfused rat heart as a model. The intraaxonal catecholamine content of adrenergic nerve fibers was visualised and morphometrically assessed by applying glyoxylic acid-induced histofluorescence. The expression of endothelial NOS in the heart was found to depend on the diameter of the blood vessel. Arteries > 100 microns always showed intense staining, whereas staining in smaller arteries and veins was considerably weaker. Smooth-muscle free vessels were essentially devoid of NADPH-d activity. In atrial and ventricular myocardium, neuronal NOS localised in autonomic nerve fibers along the entire vascular tree. Ultrastructurally, NADPH-d staining revealed adjacent localisation of NOS-positive and -negative axons, suggesting and interaxonal modulation of adjacent autonomic nerve fibers by NO. In isolated perfused rat hearts, the intracoronary application of 10(-8) M NO produced a marked decrease of coronary perfusion pressure, which was accompanied by a distinct increase in intraaxonal catecholamine levels of intramural adrenergic nerve fibers.(ABSTRACT TRUNCATED AT 250 WORDS) MESH: Adrenergic-Fibers-physiology; Amino-Acid-Oxidoreductases-analysis; Endothelium,-Vascular-enzymology; Endothelium,-Vascular-innervation; Heart-drug-effects; Heart-physiology; Muscle,-Smooth,-Vascular-physiology; Myocardium-enzymology; Myocardium-ultrastructure; Norepinephrine-metabolism; NADPH-Dehydrogenase; Rats-; Rats,-Wistar; Synaptic-Transmission-drug-effects; Vascular-Resistance-physiology MESH: *Nitric-Oxide-pharmacology; *Sympathetic-Nervous-System-physiology; *Synaptic-Transmission-physiology TG: Animal; Male PT: JOURNAL-ARTICLE RN: EC 1.14.13.39; EC 1.4.; EC 1.6.99.1; 10102-43-9; 51-41-2 NM: Nitric-Oxide-Synthase; Amino-Acid-Oxidoreductases; NADPH-Dehydrogenase; Nitric-Oxide; Norepinephrine AN: 95111174 UD: 9504 -------------------------------------------------------------------------------- Record 35 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Modulation of baroreceptor activity by ionic and paracrine mechanisms: an overview. AU: Chapleau-MW; Abboud-FM AD: Department of Veterans Affairs Medical Center, Iowa City, Iowa 52242. SO: Braz-J-Med-Biol-Res. 1994 Apr; 27(4): 1001-15 ISSN: 0100-879X PY: 1994 LA: ENGLISH CP: BRAZIL AB: 1. The primary mechanism of activation of baroreceptors is mechanical deformation during vascular stretch. In addition, baroreceptor activity is modulated by ionic mechanisms and by neurohumoral and paracrine factors that act directly on the nerve endings. 2. Ionic mechanisms play a major role in causing baroreceptor activity to decline during a sustained increase in arterial pressure (adaptation) and in the suppression of activity that occurs after pressure returns to basal levels (post-excitatory depression). Activation of a 4-aminopyridine-sensitive K+ channel contributes to adaptation, whereas activation of an electrogenic sodium pump is responsible for post-excitatory depression. 3. Factors released from vascular endothelium exert powerful effects on baroreceptor sensitivity. Prostacyclin increases baroreceptor sensitivity and contributes to baroreceptor activation during vascular stretch. Nitric oxide, endothelin and oxygen-derived free radicals suppress baroreceptor activity particularly at high levels of arterial pressure. The sympathetic neurotransmitter norepinephrine modulates baroreceptor activity: a) indirectly through its vasoconstrictor action, b) directly by binding to alpha-adrenergic receptors on the nerve endings, and c)through release of a cyclooxygenase metabolite, possibly prostacyclin, from endothelium. 4. Endothelial dysfunction contributes to baroreceptor impairment in atherosclerosis and in chronic hypertension. Loss of the excitatory influence of prostacyclin and increased formation of free radicals and possibly endothelin contribute to the baroreceptor dysfunction. Platelets aggregating at sites of endothelial damage in the carotid sinus release a stable diffusible factor that impairs baroreceptor sensitivity. 5. Therapeutic interventions may alter baroreceptor sensitivity through paracrine mechanisms. Treatment of hypertension or atherosclerosis may improve baroreceptor sensitivity by restoring endothelial function. Antiplatelet agents may enhance baroreceptor sensitivity. Antidepressant agents may decrease baroreceptor sensitivity by inhibiting prostacyclin and/or stimulating nitric oxide formation, which may contribute to dysregulation of the circulation in patients treated for depression. MESH: Atherosclerosis-physiopathology; Blood-Pressure-physiology; Carotid-Sinus-physiology; Endothelium,-Vascular-drug-effects; Hypertension-physiopathology; Na+-K+-Exchanging-ATPase-physiology; Pressoreceptors-drug-effects; Rabbits-; 4-Aminopyridine-pharmacology MESH: *Endothelium,-Vascular-physiology; *Ion-Channels-physiology; *Pressoreceptors-physiology TG: Animal; Human; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-Non-P.H.S.; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE; REVIEW; REVIEW,-TUTORIAL CN: PO1HL14388HLNHLBI RN: EC 3.6.1.37; 0; 504-24-5 NM: Na(+)-K(+)-Exchanging-ATPase; Ion-Channels; 4-Aminopyridine AN: 94372920 UD: 9412 -------------------------------------------------------------------------------- Record 36 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Evidence that the autonomic nervous system plays a major role in the L-NAME-induced hypertension in conscious rats. AU: Cunha-RS; Cabral-AM; Vasquez-EC AD: Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, Brazil. SO: Am-J-Hypertens. 1993 Sep; 6(9): 806-9 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0895-7061 PY: 1993 LA: ENGLISH CP: UNITED-STATES AB: The present study was designed to investigate the role of the autonomic nervous system in experimental hypertension induced by chronic administration of N-nitro-L-arginine methyl ester (L-NAME) in the drinking water (1 mg/mL) over 6 days. L-NAME ingestion caused a large rise in resting mean arterial pressure (MAP) (175 +/- 5 mm Hg) and heart rate (HR) (440 +/- 17 beats per minute) compared to nontreated control rats (resting MAP: 112 +/- 2 mm Hg and HR: 345 +/- 8 beats per minute). Ganglionic blockade induced by trimethaphan (5 mg/kg, intravenously) caused a significantly (P < .01) greater decrease in MAP (delta -86 +/- 7 mm Hg) compared to control rats MAP (delta -44 +/- 4 mm Hg). This strongly suggests that the level of central sympathetic tone in L-NAME-treated rats is much greater than in nontreated rats. Using atenolol and atropine alone and combined, the level of resting sympathetic drive to the heart was found to be significantly increased in L-NAME-treated rats compared to control rats. However, vagal tone to the heart was found to be virtually abolished in L-NAME-treated rats compared to control rats. These results indicate that an increase in central sympathetic drive plays an important role in the hypertension induced by chronic inhibition of nitric oxide synthesis with L-NAME. MESH: Atenolol-pharmacology; Atropine-pharmacology; Blood-Pressure-drug-effects; Ganglionic-Blockers-pharmacology; Heart-Rate-drug-effects; Hypertension-chemically-induced; Rats-; Rats,-Wistar; Trimethaphan-pharmacology; Vagus-Nerve-physiology MESH: *Arginine-analogs-and-derivatives; *Autonomic-Nervous-System-physiopathology; *Hypertension-physiopathology; *Nitric-Oxide-antagonists-and-inhibitors TG: Animal; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 0; 10102-43-9; 29122-68-7; 50903-99-6; 51-55-8; 7004-12-8; 7187-66-8 NM: Ganglionic-Blockers; Nitric-Oxide; Atenolol; NG-Nitroarginine-Methyl-Ester; Atropine; Arginine; Trimethaphan AN: 94153485 UD: 9406 -------------------------------------------------------------------------------- Record 37 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Nitric oxide synthase inhibitor inhibits catecholamines release caused by hypogastric sympathetic nerve stimulation. AU: Thatikunta-P; Chakder-S; Rattan-S AD: Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania. SO: J-Pharmacol-Exp-Ther. 1993 Dec; 267(3): 1363-8 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0022-3565 PY: 1993 LA: ENGLISH CP: UNITED-STATES AB: Recent studies suggest that nitric oxide (NO) plays a significant role in the parasympathetic inhibitory neurotransmission to the internal and sphincter (IAS). The role of NO in the sympathetic neurotransmission in the gut is not known. The resting intraluminal pressures of anesthetized opossum IAS (IASP) were monitored using low-compliance continuously perfused catheters. The plasma levels of catecholamines norepinephrine, epinephrine and dopamine were measured using a radioenzymatic assay. Parallel studies to determine the effects of hypogastric nerve stimulation (HGNS) on the resting IASP and catecholamine release were performed. The influence of NO in the sympathetic neurotransmission was determined by examining the effect of the NO synthase inhibitor L-NG-nitro-arginine (L-NNA) and the reversal of the effect by L-arginine. HGNS caused a frequency-dependent rise in the IASP accompanied by rises in norepinephrine, epinephrine and dopamine levels. The increases in the IASP and norepinephrine, epinephrine and dopamine levels were stereoselectively and significantly attenuated by L-NNA. Furthermore, the L-NNA-induced attenuation of rises in the resting IASP and catecholamine levels in response to HGNS was reversed stereoselectively by L-arginine. These studies for the first time (to the authors' knowledge) show that the NO synthase inhibitor causes specific suppression of sympathetic neurotransmitter release in the gut smooth muscle. It was concluded that, in the anorectum, NO has a facilitory role in the release of sympathetic neurotransmitters. MESH: Anus-enzymology; Arginine-analogs-and-derivatives; Arginine-pharmacology; Catecholamines-metabolism; Dopamine-metabolism; Dopamine-secretion; Electric-Stimulation; Epinephrine-metabolism; Epinephrine-secretion; Norepinephrine-metabolism; Norepinephrine-secretion; Opossums-; Sympathetic-Nervous-System-physiology MESH: *Amino-Acid-Oxidoreductases-antagonists-and-inhibitors; *Anus-innervation; *Anus-secretion; *Catecholamines-secretion; *Hypogastric-Plexus-physiology TG: Animal; Female; Male; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: DK35385DKNIDDK RN: EC 1.14.13.39; EC 1.4.; 0; 2149-70-4; 51-41-2; 51-43-4; 51-61-6; 7004-12-8 NM: Nitric-Oxide-Synthase; Amino-Acid-Oxidoreductases; Catecholamines; Nitroarginine; Norepinephrine; Epinephrine; Dopamine; Arginine AN: 94087592 UD: 9403 -------------------------------------------------------------------------------- Record 38 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: The central effects of a nitric oxide synthase inhibitor (N omega-nitro-L-arginine) on blood pressure and plasma renin. AU: el-Karib-AO; Sheng-J; Betz-AL; Malvin-RL AD: Department of Physiology, University of Michigan School of Medicine, Ann Arbor 48109. SO: Clin-Exp-Hypertens. 1993 Sep; 15(5): 819-32 ISSN: 1064-1963 PY: 1993 LA: ENGLISH CP: UNITED-STATES AB: An endothelium-derived relaxing factor has been identified as nitric oxide (NO). Peripheral and central administration of nitric oxide synthase inhibitors result in an increase in renal sympathetic nerve activity and an increase in blood pressure. The goal of our study was to determine if the increase in blood pressure following central NO synthase inhibition with N omega-nitro-L-arginine (L-NNA) is caused by the release of renin. Six groups of Sprague-Dawley rats were used. Group I (control) received intracerebroventricular (i.c.v.) artificial cerebrospinal fluid. Groups II & III received i.c.v. L-NNA, 5 & 15 micrograms/min. respectively. Group IV was treated with intravenous L-NNA, 15 micrograms/min. Group V, after bilateral nephrectomy, received i.c.v. L-NNA, 15 micrograms/min. Group VI received i.c.v. L-arginine, 60 micrograms/min. and i.c.v. L-NNA, 15 micrograms/min., simultaneously. Plasma renin concentration was measured in groups I, III, IV & V. Mean arterial blood pressure was significantly increased in groups II, III & V, i.e., following i.c.v. infusion of L-NNA. The increase in mean arterial blood pressure was significantly greater when the dose was increased from 5 to 15 micrograms/min. and it was eliminated when L-arginine was added to the infusion. The increase in blood pressure was attended by no change in heart rate. While the plasma renin concentration increased significantly in group III, this could not explain the increase in blood pressure since the nephrectomized group (V) showed no increase in renin concentration but an equivalent increase in blood pressure. The results show that acute central administration of a low dose of L-NNA increases blood pressure in rats and this increase can be prevented by central administration of L-arginine. However, intravenous infusion of the same dose (15 micrograms/min.) of L-NNA does not change blood pressure. We conclude that L-NNA acts directly within the central nervous system to increase blood pressure by a renin-independent mechanism. These results imply that central nitric oxide plays an important role in the regulation of blood pressure. MESH: Arginine-administration-and-dosage; Arginine-pharmacology; Blood-Pressure-physiology; Injections,-Intravenous; Injections,-Intraventricular; Kidney-physiology; Nephrectomy-; Rats-; Rats,-Sprague-Dawley; Sympathetic-Nervous-System-drug-effects; Sympathetic-Nervous-System-physiology MESH: *Amino-Acid-Oxidoreductases-antagonists-and-inhibitors; *Arginine-analogs-and-derivatives; *Blood-Pressure-drug-effects; *Renin-blood TG: Animal; Male; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: HL18575HLNHLBI RN: EC 1.14.13.39; EC 1.4.; EC 3.4.23.15; 2149-70-4; 7004-12-8 NM: Nitric-Oxide-Synthase; Amino-Acid-Oxidoreductases; Renin; Nitroarginine; Arginine AN: 94004766 UD: 9401 -------------------------------------------------------------------------------- Record 39 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Role of nitric oxide and angiotensin II in the regulation of sympathetic nerve activity in spontaneously hypertensive rats. AU: Kumagai-H; Averill-DB; Khosla-MC; Ferrario-CM AD: Department of Brain and Vascular Research, Cleveland Clinic Foundation, Ohio. SO: Hypertension. 1993 Apr; 21(4): 476-84 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0194-911X PY: 1993 LA: ENGLISH CP: UNITED-STATES AB: This study evaluated the actions of nitric oxide on the blood pressure and renal sympathetic nerve activity responses produced by angiotensin II (Ang II) blockade in conscious spontaneously hypertensive rats. Two days after implantation of electrodes, we measured mean arterial pressure, heart rate, and renal sympathetic nerve activity. Baroreceptor reflex function was assessed with a logistic function curve; the maximum slope of the curve estimated the baroreceptor reflex gain. Data were obtained in rats given acute intravenous administration of either vehicle, the Ang II type 1 receptor antagonist losartan, the type 2 antagonist CGP 42112A, or the converting enzyme inhibitor lisinopril. In comparison with vehicle (-1.1 +/- 0.2%/mm Hg), both losartan (-1.8 +/- 0.3%/mm Hg) and lisinopril (-2.4 +/- 0.2%/mm Hg) significantly increased the maximum gain of the baroreceptor reflex control of nerve activity (p < 0.05). In contrast, the type 2 receptor antagonist did not alter baroreceptor reflex function. Similar studies were performed in rats that received an intravenous injection of NG-monomethyl L-arginine (10 mg/kg). The nitric oxide synthase inhibitor increased baseline blood pressure and decreased renal sympathetic nerve activity. Subsequent administration of losartan or lisinopril returned blood pressure to initial hypertensive level, whereas sympathetic nerve activity was increased to a level above the initial control value. The maximum gain of the baroreceptor reflex control of renal nerve activity was increased after the nitric oxide inhibition. The present study demonstrates that blunted baroreceptor reflex function in conscious spontaneously hypertensive rats is mediated by an Ang II type 1 receptor.(ABSTRACT TRUNCATED AT 250 WORDS) MESH: Angiotensin-II-antagonists-and-inhibitors; Arginine-pharmacology; Heart-Rate-drug-effects; Pressoreceptors-physiology; Rats-; Rats,-Inbred-SHR; Reflex-drug-effects; Reflex-physiology MESH: *Angiotensin-II-physiology; *Angiotensin-Converting-Enzyme-Inhibitors-pharmacology; *Arginine-analogs-and-derivatives; *Biphenyl-Compounds-pharmacology; *Blood-Pressure-drug-effects; *Dipeptides-pharmacology; *Imidazoles-pharmacology; *Nitric-Oxide-metabolism; *Oligopeptides-pharmacology; *Receptors,-Angiotensin-antagonists-and-inhibitors; *Tetrazoles-pharmacology TG: Animal; Male; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: HL6835HLNHLBI RN: 0; 0; 0; 0; 0; 0; 0; 10102-43-9; 11128-99-7; 114798-26-4; 127060-75-7; 17035-90-4; 7004-12-8; 83915-83-7 NM: Angiotensin-Converting-Enzyme-Inhibitors; Biphenyl-Compounds; Dipeptides; Imidazoles; Oligopeptides; Receptors,-Angiotensin; Tetrazoles; Nitric-Oxide; Angiotensin-II; losartan; CGP-42112A; omega-N-Methylarginine; Arginine; Lisinopril AN: 93209695 UD: 9307 -------------------------------------------------------------------------------- Record 40 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Inhibition of nitric oxide formation in the nucleus tractus solitarius increases renal sympathetic nerve activity in rabbits. AU: Harada-S; Tokunaga-S; Momohara-M; Masaki-H; Tagawa-T; Imaizumi-T; Takeshita-A AD: Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan. SO: Circ-Res. 1993 Mar; 72(3): 511-6 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0009-7330 PY: 1993 LA: ENGLISH CP: UNITED-STATES AB: It has been shown that nitric oxide (NO) is synthesized in the central nervous system as well as in vascular endothelial cells. However, the physiological role of NO in cardiovascular regulation by the central nervous system remains unclear. This objective of this study was to examine the possibility that NO plays a role in neural transmission in the nucleus tractus solitarius (NTS) and thus contributes to control of sympathetic nerve activity in rabbits. We examined the effects of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of the formation of NO from L-arginine, microinjected into the NTS on arterial pressure (AP), heart rate (HR), and renal sympathetic nerve activity (RSNA). L-NMMA increased AP and RSNA in rabbits with intact as well as denervated sinoaortic baroreceptors and vagi. L-NMMA increased HR only in rabbits with sinoaortic denervation and vagotomy. Pretreatment with L-arginine microinjected into the NTS, which did not alter baseline AP, HR, and RSNA, prevented the increases in AP and RSNA evoked with subsequent L-NMMA. Pretreatment with D-arginine did not alter the effects of subsequent L-NMMA injections into the NTS. The gain of arterial baroreflex control of RSNA assessed by the slope of the regression line relating changes in AP and those in RSNA caused by intravenous phenylephrine or nitroglycerin did not differ before and after microinjections of L-NMMA. L-NMMA microinjected into the area postrema did not alter AP, HR, or RSNA. These results suggest that in rabbits NO is involved in the mechanism in the NTS that mediates tonic inhibition of RSNA.(ABSTRACT TRUNCATED AT 250 WORDS) MESH: Arginine-pharmacology; Arteries-; Blood-Pressure-drug-effects; Cerebellum-metabolism; Denervation-; Heart-Rate-drug-effects; Pressoreceptors-drug-effects; Rabbits- MESH: *Arginine-analogs-and-derivatives; *Cerebellum-drug-effects; *Kidney-innervation; *Nitric-Oxide-antagonists-and-inhibitors; *Sympathetic-Nervous-System-drug-effects TG: Animal; Comparative-Study; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 10102-43-9; 17035-90-4; 7004-12-8 NM: Nitric-Oxide; omega-N-Methylarginine; Arginine AN: 93161485 UD: 9305 -------------------------------------------------------------------------------- Record 41 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Renal vasoconstriction is modulated by nitric oxide. AU: Reid-JJ; Rand-MJ AD: Department of Pharmacology, University of Melbourne, Victoria, Australia. SO: Clin-Exp-Pharmacol-Physiol. 1992 May; 19(5): 376-9 ISSN: 0305-1870 PY: 1992 LA: ENGLISH CP: ENGLAND AB: 1. The effect of the nitric oxide synthesis inhibitor, NG-nitro-L-arginine (NOLA), has been examined on vascular reactivity in the rat isolated perfused kidney. 2. NOLA (10 mumol/L) had no effect on basal perfusion pressure, but significantly enhanced the vasoconstrictor responses to sympathetic nerve stimulation (1-16 Hz, 10 s) and noradrenaline (10-300 pmol). The enhancements were greater with the lower frequencies of stimulation and lower doses of noradrenaline. 3. The enhancing effect of 10 mumol/L NOLA on vasoconstrictor responses to nerve stimulation was partially prevented by 100 mumol/L L-arginine while 100 mumol/L D-arginine had no effect. 4. The results suggest that nitric oxide attenuates vasoconstrictor responses in the rat kidney, and provide evidence that nitric oxide has a physiological role in the modulation of vascular reactivity. MESH: Arginine-analogs-and-derivatives; Arginine-pharmacology; Electric-Stimulation; Norepinephrine-pharmacology; Perfusion-; Rats-; Rats,-Inbred-Strains; Sympathetic-Nervous-System-physiology; Time-Factors; Vasoconstriction-drug-effects MESH: *Kidney-blood-supply; *Nitric-Oxide-pharmacology; *Vasoconstriction-physiology TG: Animal; Female; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 10102-43-9; 2149-70-4; 51-41-2; 7004-12-8 NM: Nitric-Oxide; Nitroarginine; Norepinephrine; Arginine AN: 92393860 UD: 9212 -------------------------------------------------------------------------------- Record 42 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Nitric oxide from endothelium and smooth muscle modulates responses to sympathetic nerve stimulation: implications for endotoxin shock. AU: Gonzalez-C; Fernandez-A; Martin-C; Moncada-S; Estrada-C AD: Department of Physiology, School of Medicine, Universidad Autonoma de Madrid, Spain. SO: Biochem-Biophys-Res-Commun. 1992 Jul 15; 186(1): 150-6 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0006-291X PY: 1992 LA: ENGLISH CP: UNITED-STATES AB: The influence of nitric oxide (NO) on vascular responses to transmural stimulation (TNS) of noradrenergic nerves was studied in isolated rings of rat iliac arteries. TNS produced frequency-dependent contractions in all vessels. The NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) significantly enhanced TNS responses in intact vessels, but not in those in which the endothelium had been removed. However, in endothelium-denuded rings incubated for 8 hours, L-NMMA increased the contractions induced by nerve stimulation, an effect which was prevented by treatment with dexamethasone or cycloheximide, and enhanced by incubation with lipopolysaccharide and gamma-interferon. Addition of L-arginine reversed the effect of L-NMMA in intact rings; however, it significantly decreased below control values TNS-induced contractions in vessels without endothelium. The results indicate that a) the arterial response to noradrenergic nerve stimulation is modulated by NO originating either in endothelial cells or in smooth muscle cells after induction of NO synthase activity, and b) once NO synthase is induced, the limiting step in NO production is the availability of the substrate L-arginine. An overproduction of vascular NO in the presence of endotoxin or other inflammatory stimuli may prevent the vascular response to sympathetic stimuli and contribute to the vasodilation observed in inflammation or endotoxic shock. MESH: Acetylcholine-pharmacology; Arginine-pharmacology; Cycloheximide-pharmacology; Dexamethasone-pharmacology; Dinoprost-pharmacology; Endotoxins-pharmacology; Iliac-Artery-drug-effects; Interferon-Type-II-pharmacology; Isometric-Contraction-drug-effects; Muscle,-Smooth,-Vascular-drug-effects; Phentolamine-pharmacology; Prazosin-pharmacology; Rats-; Rats,-Inbred-Strains MESH: *Arginine-analogs-and-derivatives; *Endothelium,-Vascular-physiology; *Iliac-Artery-physiology; *Muscle,-Smooth,-Vascular-physiology; *Nitric-Oxide-metabolism; *Shock,-Septic-physiopathology TG: Animal; In-Vitro; Male; Support,-Non-U.S.-Gov't PT: JOURNAL-ARTICLE RN: 0; 10102-43-9; 17035-90-4; 19216-56-9; 50-02-2; 50-60-2; 50903-99-6; 51-84-3; 551-11-1; 66-81-9; 7004-12-8; 82115-62-6 NM: Endotoxins; Nitric-Oxide; omega-N-Methylarginine; Prazosin; Dexamethasone; Phentolamine; NG-Nitroarginine-Methyl-Ester; Acetylcholine; Dinoprost; Cycloheximide; Arginine; Interferon-Type-II AN: 92337589 UD: 9210 -------------------------------------------------------------------------------- Record 43 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: NG-methyl-L-arginine, an inhibitor of L-arginine-derived nitric oxide synthesis, stimulates renal sympathetic nerve activity in vivo. A role for nitric oxide in the central regulation of sympathetic tone? AU: Sakuma-I; Togashi-H; Yoshioka-M; Saito-H; Yanagida-M; Tamura-M; Kobayashi-T; Yasuda-H; Gross-SS; Levi-R AD: Department of Cardiovascular Medicine, School of Medicine, Hokkaido University, Sapporo, Japan. SO: Circ-Res. 1992 Mar; 70(3): 607-11 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0009-7330 PY: 1992 LA: ENGLISH CP: UNITED-STATES AB: Continuous production of endothelium-derived nitric oxide (NO) in peripheral vessels has been shown to modulate vascular resistance and blood pressure. NO is also formed in the brain upon activation of glutamate receptors, which are thought to mediate central autonomic reflexes. In the present study we assessed whether NO plays a role in central autonomic regulation. For this, we have investigated the effects of NG-methyl-L-arginine (NMA), a selective inhibitor of NO synthesis from L-arginine, on sympathetic renal nerve activity (RNA), blood pressure, and heart rate in the anesthetized rat. NMA elicited a dose-dependent sustained increase in blood pressure (approximately 20 and 30 mm Hg, 5 minutes after 10 and 50 mumol/kg i.v., respectively). Heart rate and RNA decreased transiently (15 beats per minute and 40%, respectively); RNA subsequently increased (100%) while blood pressure remained elevated. Baroreceptor deafferentation markedly altered these responses to NMA; the transient decreases in heart rate and RNA were abolished, whereas the increases in RNA and blood pressure were significantly potentiated. After spinal C-1-C-2 transection, there was no increase in RNA, and blood pressure increased to a smaller extent. L-Arginine blocked the NMA-induced increases in blood pressure and RNA. Thus, in addition to modulating vascular resistance by a peripheral action, NO may also play a role in the central regulation of sympathetic tone. MESH: Arginine-pharmacology; Blood-Pressure-drug-effects; Heart-Rate-drug-effects; Homeostasis-; Neural-Conduction; Neural-Inhibition; Rats-; Rats,-Inbred-Strains; Vagotomy- MESH: *Arginine-analogs-and-derivatives; *Arginine-antagonists-and-inhibitors; *Kidney-innervation; *Nitric-Oxide-metabolism; *Sympathetic-Nervous-System-drug-effects TG: Animal; Comparative-Study; Male; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: HL34215HLNHLBI RN: 10102-43-9; 17035-90-4; 7004-12-8 NM: Nitric-Oxide; omega-N-Methylarginine; Arginine AN: 92164034 UD: 9206 -------------------------------------------------------------------------------- Record 44 of 44 - MEDLINE EXPRESS (R) 1992-1996 TI: Effect of endothelium on the actions of sympathetic and sensory nerves in the perfused rat mesentery. AU: Li-YJ; Duckles-SP AD: Department of Pharmacology, College of Medicine, University of California, Irvine 92717. SO: Eur-J-Pharmacol. 1992 Jan 7; 210(1): 23-30 *LHM: Bestand in der Charit‚ -> siehe Zeitschriftenkatalog! ISSN: 0014-2999 PY: 1992 LA: ENGLISH CP: NETHERLANDS AB: We and others have previously demonstrated that pretreatment with capsaicin produces an augmentation of vasoconstrictor responses to transmural nerve stimulation. In the present study, removal of endothelium by saponin or inhibition of nitric oxide synthesis by N omega-nitro-L-arginine methyl ester produced an augmentation of vasoconstrictor responses to transmural nerve stimulation, responses which were further potentiated after treatment with capsaicin to desensitize sensory nerves. Capsaicin treatment decreased vasodilator responses to acetylcholine, but only at low acetylcholine concentrations. Potentiation by capsaicin of vasoconstrictor responses to transmural nerve stimulation was not affected by indomethacin. In the presence of guanethidine and methoxamine, transmural nerve stimulation caused vasodilator responses in the perfused rat mesentery. These responses were unaffected by removal of endothelium, as were vasodilator responses to exogenous calcitonin gene-related peptide (CGRP). In contrast, substance P did not produce any relaxation in the methoxamine-contracted mesentery. This study suggests that facilitation of vasoconstrictor responses to transmural nerve stimulation after capsaicin treatment primarily reflects inhibition of sensory nerve effects resulting in an increase of sympathetic vasoconstrictor actions. The present results also suggest that vasodilator responses to sensory nerve activation or exogenous CGRP are endothelium-independent and that substance P does not significantly contribute to modulation of vascular tone in the rat mesentery. MESH: Acetylcholine-pharmacology; Calcitonin-Gene-Related-Peptide-pharmacology; Capsaicin-pharmacology; Electric-Stimulation; Endothelium,-Vascular-innervation; Muscle-Relaxation-drug-effects; Muscle,-Smooth,-Vascular-innervation; Perfusion-; Rats-; Rats,-Inbred-Strains; Substance-P-pharmacology; Vasoconstriction- MESH: *Endothelium,-Vascular-physiology; *Mesenteric-Arteries-innervation; *Neurons,-Afferent-physiology; *Sympathetic-Nervous-System-physiology TG: Animal; Male; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S. PT: JOURNAL-ARTICLE CN: P01DK36289DKNIDDK RN: 33507-63-0; 404-86-4; 51-84-3; 83652-28-2 NM: Substance-P; Capsaicin; Acetylcholine; Calcitonin-Gene-Related-Peptide AN: 92289861 UD: 9209