UI - 97222200 AU - Stauss HM AU - Morgan DA AU - Anderson KE AU - Massett MP AU - Kregel KC TI - Modulation of baroreflex sensitivity and spectral power of blood pressure by heat stress and aging. LA - Eng MH - Aging/*physiology MH - Animal MH - Baroreflex/*physiology MH - Blood Pressure/*physiology MH - Heart Rate MH - *Heat MH - Hemodynamics MH - Rats MH - Rats, Inbred F344 MH - Stress/*physiopathology MH - Support, Non-U.S. Gov't MH - Support, U.S. Gov't, P.H.S. PT - JOURNAL ARTICLE ID - AG-12350/AG/NIA DA - 970422 DP - 1997 Feb IS - 0002-9513 TA - Am J Physiol PG - H776-84 SB - M CY - UNITED STATES IP - 2 Pt 2 VI - 272 JC - 3U8 AA - Author EM - 9706 AB - To investigate the effects of hyperthermia and aging on baroreceptor- heart rate reflex sensitivity (BRS), cardiovascular parameters were recorded during a progressive rise in core temperature in conscious mature and senescent Fischer 344 rats. BRS was calculated from spontaneous changes in blood pressure and interbeat interval. Low- (LF, 0.01-0.20 Hz) and mid- (MF, 0.2-0.5 Hz) frequency blood pressure power were also determined. In both age groups, hyperthermia caused an increase in blood pressure, renal resistance, and LF but no changes in renal nerve activity, whereas a tachycardia was only observed in the older rats. Increases in BRS (0.80 +/- 0.14 vs. 1.72 +/- 0.34 ms/mmHg, P < 0.05) and MF (3.10 +/- 0.55 vs. 7.81 +/- 1.89 mmHg2, P < 0.05) and a positive correlation between BRS and MF (r = 0.50, P < 0.01) were observed with heating in mature but not senescent rats. These results indicate that LF, which increased with elevated core temperature, may be modulated by thermal stimuli. The augmented BRS in the mature group may contribute to the hemodynamic adjustments that occur with hyperthermia, whereas the lack of an increase in BRS during heat stress in the senescent group suggests that baroreceptor reflex modulation is impaired with aging. The positive correlation between BRS and MF in mature rats, together with the lack of an increase in renal sympathetic nerve activity, indicates that MF may reflect the modulating influence of the efferent sympathetic portion of the baroreceptor reflex loop on arterial blood pressure rather than merely the activity of the peripheral sympathetic nervous system. AD - Department of Exercise Science, The University of Iowa, Iowa City 52242, USA. PMID- 9124438 SO - Am J Physiol 1997 Feb;272(2 Pt 2):H776-84 UI - 97053484 AU - Patzak A AU - Lipke K AU - Orlow W AU - Mrowka R AU - Stauss H AU - Windt E AU - Persson PB AU - Schubert E TI - Development of heart rate power spectra reveals neonatal peculiarities of cardiorespiratory control. LA - Eng MH - Aging/physiology MH - Female MH - Fourier Analysis MH - Heart/*physiology MH - *Heart Rate MH - Human MH - Infant MH - Infant, Newborn/*physiology MH - Male MH - Respiration/*physiology MH - Support, Non-U.S. Gov't PT - JOURNAL ARTICLE DA - 961216 DP - 1996 Oct IS - 0002-9513 TA - Am J Physiol PG - R1025-32 SB - M CY - UNITED STATES IP - 4 Pt 2 VI - 271 JC - 3U8 AA - Author EM - 9702 AB - Postnatal adaptation should be associated with changes in cardiac rhythmic behavior. To examine the development of heart rate variability, instantaneous heart rate (IHR) and the corresponding breathing signals of 16 healthy infants were analyzed. This was pursued by use of fast Fourier transformation beginning with the 1st day until the 6th mo of life. Power in the low-frequency range (LF, 0.02-0.2 Hz) and high-frequency range (HF, 0.2-1.5 Hz), total power (TP), the quotient LF/HF, and the frequency of the peak in LF and HF (LFF and HFF, respectively) were derived from the IHR spectrum. The peak frequency in HF (RF) was detected in the respiratory spectrum. Power and frequency of IHR rhythms undergo a marked development. TP, LF, and HF are lowest from the end of the 1st mo until the 2nd mo. LF predominates over HF, with LF/HF reaching its peak during 1- to 2-mo period. HF, recording respiratory related rhythms is negatively correlated with the breathing rate (BR). HFF and RF both show an increasing tendency during the 1st mo followed by a decrease down to the 6th mo. However, HFF is lower than RF if BR is high, mainly during the first 2 mo. The distinct changes in BR and its important influence on the IHR spectrum underscore the importance of monitoring respiration as a further measure in the diagnosis of infants. LFF is on average between 0.075 and 0.095 Hz, exhibiting an irregular course with minimum at the 10th, 21st-28th, and 90th day being apparent. The developmental pattern of LFF may by interpreted in terms of the maturation of the nervous system involved in the generation of circulatory rhythms. AD - Department of Neonatology, Humboldt University of Berlin, University Hospital Charite, Germany. patzak@rz.charite.hu-berlin.de PMID- 8897996 SO - Am J Physiol 1996 Oct;271(4 Pt 2):R1025-32 UI - 97053423 AU - Stauss HM AU - Kregel KC TI - Frequency response characteristic of sympathetic-mediated vasomotor waves in conscious rats. LA - Eng MH - Anesthesia MH - Animal MH - Blood Pressure MH - Electric Stimulation MH - Heart Rate MH - Hemodynamics MH - Male MH - Rats MH - Rats, Sprague-Dawley MH - Splanchnic Circulation MH - Support, Non-U.S. Gov't MH - Support, U.S. Gov't, P.H.S. MH - Sympathetic Nervous System/*physiology MH - Vascular Resistance MH - Vasomotor System/*physiology PT - JOURNAL ARTICLE ID - AG-12350/AG/NIA DA - 961216 DP - 1996 Oct IS - 0002-9513 TA - Am J Physiol PG - H1416-22 SB - M CY - UNITED STATES IP - 4 Pt 2 VI - 271 JC - 3U8 AA - Author EM - 9702 AB - Power spectrum analysis of arterial blood pressure (BP) and heart rate (HR) has been used to investigate autonomic nervous system activity. Sympathetic-mediated vasomotor tone has been attributed to the BP power at frequencies between 0.05 and 0.15 Hz in humans and dogs and between 0.2 and 0.8 Hz in rats. In contrast, it has been suggested that the sympathetic nervous system is too sluggish to transmit frequencies higher than 0.017 Hz in dogs. Thus we investigated the frequency- response characteristics of the transmission of peripheral sympathetic nerve discharge to peripheral vascular resistance and arterial blood pressure in conscious rats. Eleven rats were instrumented with arterial catheters, nerve electrodes on the sympathetic splanchnic nerve, and flow probes on the superior mesenteric artery. The splanchnic nerve was cut proximal to the electrode to avoid afferent nerve stimulation. The next day the nerve was stimulated at frequencies of 0.05, 0.1, 0.2, 0.5, 1.0, and 2.0 Hz while mesenteric blood flow, BP, and HR were recorded in conscious rats. Mesenteric resistance (MR) was calculated off-line. Nerve stimulation at 0.05, 0.1, 0.2, 0.5, and 1.0 Hz significantly increased the power in MR at these respective frequencies. The greatest response was found between 0.2 and 0.5 Hz. These oscillations in MR were translated to oscillations in BP, but not in HR. Nerve stimulation on the second day, when the nerve was degenerated, did not elicit oscillations in MR or BP. We conclude that the peripheral sympathetic nervous system in rats can transmit signals at frequencies higher than those traditionally assigned to sympathetic vasomotor activity in several species, including humans, and may even overlap with the respiration-related high-frequency range. AD - Department of Exercise Science, University of Iowa, Iowa City 52242, USA. PMID- 8897935 SO - Am J Physiol 1996 Oct;271(4 Pt 2):H1416-22 UI - 96365944 AU - Stauss HM AU - Morgan DA AU - Anderson KE AU - Massett MP AU - Kregel KC TI - Aging is not accompanied by sympathetic hyperresponsiveness to air-jet stress. LA - Eng MH - Aging/*physiology MH - Air MH - Animal MH - Blood Pressure MH - Cardiovascular System/physiopathology MH - Heart Rate MH - Kidney/*innervation MH - Physical Stimulation MH - Rats MH - Rats, Inbred F344 MH - *Renal Circulation/physiology MH - Stress/*physiopathology MH - Support, Non-U.S. Gov't MH - Support, U.S. Gov't, P.H.S. MH - Sympathetic Nervous System/*physiopathology PT - JOURNAL ARTICLE ID - AG-12350/AG/NIA DA - 961030 DP - 1996 Aug IS - 0002-9513 TA - Am J Physiol PG - H768-75 SB - M CY - UNITED STATES IP - 2 Pt 2 VI - 271 JC - 3U8 AA - Author EM - 9701 AB - It has been postulated that sympathetic nervous system reactivity to acutely applied stress is increased with age. We investigated the autonomic and hemodynamic adjustments to air-jet stress in 9 mature (12- mo-old) and 11 senescent (24-mo-old) Fischer 344 rats. Rats were instrumented with arterial and venous catheters, flow probes around the renal artery, and nerve electrodes on the ipsilateral renal nerve. After the rats recovered from surgery, blood pressure, heart rate, renal blood flow, and renal sympathetic nerve activity were recorded during control conditions and during an 8-min continuous air-jet application. Renal resistance and the low (0.01-0.20 Hz)- and mid- frequency (0.20-0.50 Hz) power of blood pressure were computed off- line. The air jet induced an increase in blood pressure, heart rate, renal resistance, renal nerve activity, and blood pressure power in the low- and mid-frequency ranges in both groups. Blood pressure and low- frequency blood pressure power increased less, and the elevations in renal resistance and renal nerve activity were of shorter duration in senescent compared with mature rats. These data suggest that sympathetic responsiveness to air-jet stress is not enhanced with increasing age. AD - Department of Exercise Science, University of Iowa, Iowa City 52242, USA. PMID- 8770121 SO - Am J Physiol 1996 Aug;271(2 Pt 2):H768-75 UI - 96253770 AU - Nafz B AU - Just A AU - Stauss HM AU - Wagner CD AU - Ehmke H AU - Kirchheim HR AU - Persson PB TI - Blood-pressure variability is buffered by nitric oxide. LA - Eng MH - Animal MH - Baroreflex/*drug effects MH - Blood Pressure/*drug effects MH - Denervation MH - Dogs MH - Nitric Oxide/*pharmacology RN - 10102-43-9 (Nitric Oxide) PT - JOURNAL ARTICLE DA - 961203 DP - 1996 Mar 7 IS - 0165-1838 TA - J Auton Nerv Syst PG - 181-3 SB - M CY - NETHERLANDS IP - 3 VI - 57 JC - H97 AA - Author EM - 9702 AB - The baroreflex constitutes the only hitherto known buffer of rapid blood pressure oscillations. In order to investigate the influence of nitric oxide (NO) and the sinoaortic and cardiopulmonary baroreflex pathways on the dynamic properties of blood pressure control, we determined the power spectra of 24-h blood pressure time series of conscious dogs. This was done in the intact state (n = 6), during blockade of NO synthesis via the false substrate NG-nitro-L-arginine ((L-NNA), 16.5 +/- 2 mg/kg body weight i.v., n = 5) and in animals devoid of baroreceptor reflexes (n = 5). After L-NNA, blood pressure (BP) increased by roughly 20 mmHg to 137 +/- 6 mmHg (P < 0.01), heart rate decreased from 97 +/- 6 to 68 +/- 3 beats/min (P < 0.01). The power of blood pressure variations within the frequency range 0.1-0.5 Hz was tripled by L-NNA (P < 0.05). By comparison total sinoaortic and cardiopulmonary denervation increased power of slower oscillations ( < 0.1 Hz) by a factor of 4.7 (P < 0.05). Thus, NO and the baroreceptor reflex both play an important role as physiological blood pressure buffers, NO for rapid (0.1-0.5 Hz) and the baroreflex for slower fluctuations ( < 0.1 Hz). AD - Physiologisches Institut, Humboldt Universitat zu Berlin (Charite), Germany. PMID- 8964946 SO - J Auton Nerv Syst 1996 Mar 7;57(3):181-3 UI - 96050114 AU - Stauss HM AU - Mrowka R AU - Nafz B AU - Patzak A AU - Unger T AU - Persson PB TI - Does low frequency power of arterial blood pressure reflect sympathetic tone? LA - Eng MH - Adrenergic alpha-Antagonists/pharmacology MH - Animal MH - Animals, Transgenic MH - Blood Pressure/*physiology MH - Comparative Study MH - Electrophysiology MH - Heart Rate/physiology MH - Mice MH - Rats MH - Rats, Inbred SHR MH - Rats, Inbred WKY MH - Rats, Sprague-Dawley MH - Receptors, Adrenergic, alpha-1/antagonists & inhibitors MH - Splanchnic Nerves/physiology MH - Support, Non-U.S. Gov't MH - Sympathetic Nervous System/*physiology RN - 0 (Adrenergic alpha-Antagonists) RN - 0 (Receptors, Adrenergic, alpha-1) PT - JOURNAL ARTICLE DA - 960117 DP - 1995 Aug 4 IS - 0165-1838 TA - J Auton Nerv Syst PG - 145-54 SB - M CY - NETHERLANDS IP - 2 VI - 54 JC - H97 AA - Author EM - 9603 AB - We tested whether power spectral analysis of arterial blood pressure (ABP) is a feasible tool to detect differences in peripheral sympathetic nerve activity in normotensive and hypertensive rats with differing basal sympathetic tones. Nine Wistar Kyoto rats (WKY), 10 Sprague-Dawley rats (SD), 10 spontaneously hypertensive rats (SHR) and 9 hypertensive transgenic rats harbouring the mouse Ren-2 gene (TGR) were chronically instrumented with femoral artery catheters and nerve electrodes around the sympathetic major splanchnic nerve. Two days after surgery ABP and splanchnic nerve activity (SpNA) were recorded in the conscious state during basal conditions as well as during alpha 1- adrenergic receptor blockade. Power spectra and squared coherence in the low (LF, 0.02-0.20 Hz), mid (MF, 0.20-0.80 Hz) and high (HF, respiration peak +/- 0.3 Hz) frequency bands were calculated for ABP and SpNA. Mean blood pressure in SHR (133 +/- 8 mmHg) and TGR (142 +/- 8 mmHg) was significantly higher (P < 0.05) than in WKY (115 +/- 3 mmHg) and SD (95 +/- 4 mmHg). SpNA in SHR was higher than in WKY (23.4 +/- 6.4 microV vs. 11.6 +/- 0.8 microV, P < 0.05) while SpNA in TGR was lower than in SD (20.1 +/- 3.9 microV vs. 28.8 +/- 4.2 microV, P < 0.05). LF and MF components of ABP variability were not significantly higher in those rats with high sympathetic tones. However, alpha 1- adrenergic receptor blockade reduced LF and MF components of ABP and SpNA in all strains except SHR. LF and MF coherence was not greater in rats with high sympathetic tones than in those with low sympathetic tones. The reduction of LF and MF components of ABP variability by alpha 1-adrenergic receptor blockade indicates an important contribution of peripheral sympathetic nerve activity to LF and MF blood pressure variability on an acute basis. However, the lack of higher LF and MF power in the ABP spectra of those rats with high SpNA together with the finding that LF and MF coherence was not higher in those rats with high SpNA led to the conclusion that LF and MF spectral components of ABP do not appear to be suitable markers for the prevailing sympathetic nerve activity. AD - Department of Physiology, Humboldt University of Berlin (Charite), Germany. PMID- 7499726 SO - J Auton Nerv Syst 1995 Aug 4;54(2):145-54 UI - 96113998 AU - Zhu YC AU - Stauss HM AU - Bao G AU - Gohlke P AU - Zhu YZ AU - Redlich T AU - Unger T TI - Role of bradykinin in the antihypertensive and cardioprotective actions of converting enzyme inhibitors. LA - Eng MH - Angiotensin-Converting Enzyme Inhibitors/*pharmacology MH - Animal MH - Antihypertensive Agents/*pharmacology MH - Bradykinin/*physiology MH - Endothelium, Vascular/drug effects MH - Heart/*drug effects MH - Human MH - Hypertrophy, Left Ventricular/prevention & control MH - Myocardial Ischemia/prevention & control RN - 0 (Angiotensin-Converting Enzyme Inhibitors) RN - 0 (Antihypertensive Agents) RN - 58-82-2 (Bradykinin) PT - JOURNAL ARTICLE PT - REVIEW PT - REVIEW, TUTORIAL DA - 961023 DP - 1995 Jul IS - 0008-4212 TA - Can J Physiol Pharmacol PG - 827-31 SB - M CY - CANADA IP - 7 VI - 73 JC - CJM AA - Author EM - 9612 AB - Angiotensin converting enzyme inhibitors (ACEIs) not only reduce angiotensin II synthesis but also potentiate endogenous kinins. In addition to their antihypertensive actions, accumulated evidence has demonstrated an improvement by ACEIs of cardiac function, cardiac structural and metabolic status, and myocardial blood flow in conditions such as cardiac ischemia, left ventricular hypertrophy, and myocardial infarction. The mechanisms underlying the antihypertensive and cardioprotective actions of ACEIs are under intensive investigation. A reduction of angiotensin II synthesis is undoubtedly responsible for a major part of the antihypertensive effects of ACEIs. However, in experimental renal hypertension but not in genetic hypertension, bradykinin potentiation has been shown to partially mediate the acute and chronic antihypertensive actions of these drugs. In addition, experimental observations suggest that bradykinin potentiation plays a pivotal role in the cardioprotective effects of ACEIs. AD - Department of Pharmacology, Christian-Albrechts Universitat zu Kiel, Germany. RF - 39 PMID- 8846416 SO - Can J Physiol Pharmacol 1995 Jul;73(7):827-31 UI - 95406038 AU - Wagner J AU - Wystrychowski A AU - Stauss H AU - Ganten D AU - Ritz E TI - Decreased renal haemodynamic response to inhibition of nitric oxide synthase in subtotally nephrectomized rats. LA - Eng MH - Amino Acid Oxidoreductases/*antagonists & inhibitors MH - Animal MH - Arginine/analogs & derivatives/administration & dosage/pharmacology MH - Blood Flow Velocity MH - Blood Pressure/drug effects MH - Dose-Response Relationship, Drug MH - Glomerular Filtration Rate MH - *Hemodynamics MH - Kidney/*blood supply MH - Male MH - *Nephrectomy MH - Nitric Oxide/pharmacology MH - Nitroprusside/pharmacology MH - Rats MH - Rats, Sprague-Dawley MH - Vascular Resistance/drug effects RN - EC 1.14.13.39 (Nitric-Oxide Synthase) RN - EC 1.4. (Amino Acid Oxidoreductases) RN - 10102-43-9 (Nitric Oxide) RN - 15078-28-1 (Nitroprusside) RN - 2149-70-4 (Nitroarginine) RN - 7004-12-8 (Arginine) PT - JOURNAL ARTICLE DA - 951019 DP - 1995 Jun IS - 0031-6768 TA - Pflugers Arch PG - 181-7 SB - M CY - GERMANY IP - 2 VI - 430 JC - OZX AA - Author EM - 9512 AB - To assess the renal haemodynamic response to manipulations of the nitric oxide (NO) system, we examined subtotally nephrectomized (SNX) rats and control rats (CON) 28 days after their operation. Bolus infusions of the NO synthase inhibitor NG-nitro-L-arginine (L-NA) were given intravenously at doses of 2 mg/kg and 10 mg/kg. Blood pressure was measured intra-arterially, glomerular filtration rate was measured by inulin clearance and fractional changes in renal blood flow (RBF) were determined by a Doppler flow probe. Both doses of L-NA caused a similar and dose-dependent increase in mean blood pressure in both SNX and CON rats. In contrast, the decrease in RBF and the increase in the renovascular resistance index (RVRI) was less in SNX rats as compared to CON rats (RBF = -70.1 +/- 2.2% of baseline vs -52.7 +/- 5.2%, P < 0.01; RVRI = +177 +/- 9% of baseline vs +243 +/- 24%, P < 0.05). These changes were not affected by autonomic blockade (hexamethonium), or by blockade of the angiotensin II receptor (Losartan). The exogenous NO donor sodium nitroprusside (0.5 and 1.5 micrograms.kg-1.min-1) lowered mean blood pressure to a similar degree in SNX and CON rats; in contrast, RVRI decreased less in SNX rats (86.9 +/- 9.2% of baseline) than in CON rats (68.2 +/- 4.6%, P < 0.05). We conclude that the reaction of the renal vasculature to manipulations of the NO system is altered in the SNX rats.(ABSTRACT TRUNCATED AT 250 WORDS) AD - Department of Nephrology, University of Heidelberg, Germany. PMID- 7545811 CU - 96 SO - Pflugers Arch 1995 Jun;430(2):181-7 UI - 95146130 AU - Falkenhahn M AU - Franke F AU - Bohle RM AU - Zhu YC AU - Stauss HM AU - Bachmann S AU - Danilov S AU - Unger T TI - Cellular distribution of angiotensin-converting enzyme after myocardial infarction. LA - Eng MH - Adult MH - Aged MH - Animal MH - Antibodies, Monoclonal MH - Female MH - Human MH - Immunohistochemistry/methods MH - Male MH - Middle Age MH - Myocardial Infarction/*metabolism/pathology MH - Myocardium/*metabolism/pathology MH - Peptidyl-Dipeptidase A/*metabolism MH - Rats MH - Rats, Wistar MH - Staining MH - Time Factors MH - Tissue Distribution RN - EC 3.4.15.1 (Peptidyl-Dipeptidase A) RN - 0 (Antibodies, Monoclonal) PT - JOURNAL ARTICLE DA - 950306 DP - 1995 Feb IS - 0194-911X TA - Hypertension PG - 219-26 SB - M CY - UNITED STATES IP - 2 VI - 25 JC - GK7 AA - Author EM - 9505 AB - We studied the cellular distribution of angiotensin-converting enzyme (ACE) in the heart related to the cell types involved in left ventricular repair and remodeling before and after myocardial infarction by immunohistochemical techniques using monoclonal and polyclonal antibodies. In noninfarcted myocardium of both human and rat, ACE expression was confined to endothelial cells and subendocardial cell layers of the aortic valve. ACE was prominent in endothelia of small arteries and arterioles, whereas only half the coronary capillaries were immunoreactive and venous vessels were almost completely devoid of the enzyme. In a rat model of myocardial infarction, ACE distribution was determined 1, 3, and 7 days and 2, 3, and 6 weeks after coronary occlusion. Three and 7 days after infarction, endothelial cells of sprouting capillaries and macrophages in the marginal zone of necrosis revealed ACE expression. In both human and rat with the onset of fibrosis, intense staining of the enzyme was found in the marginal zone of the repair tissue. In situ hybridization for collagen type I in the rat revealed that zones with high collagen content had almost no ACE immunoreactivity. Vascular smooth muscle cells and cardiomyocytes revealed no ACE expression throughout the study. We conclude that endothelial cells are the principal source for the expression of ACE after myocardial infarction. The observed induction of ACE with the onset of fibrosis suggests a role of this enzyme that is related to tissue repair and remodeling. AD - Department of Pharmacology, University of Kiel, Germany. PMID- 7531176 CU - 95 SO - Hypertension 1995 Feb;25(2):219-26 UI - 95219931 AU - Stauss HM AU - Persson PB TI - Power spectral analysis of heart rate and blood pressure: markers for autonomic balance or indicators of baroreflex control? [comment] LA - Eng MH - Autonomic Nervous System/*physiology MH - Baroreflex/*physiology MH - Blood Pressure/*physiology MH - Cardiovascular Diseases/physiopathology MH - Heart Rate/*physiology MH - Human MH - Monitoring, Physiologic MH - Signal Processing, Computer-Assisted PT - COMMENT PT - JOURNAL ARTICLE PT - REVIEW PT - REVIEW, TUTORIAL DA - 950511 DP - 1995 Jan IS - 0143-5221 TA - Clin Sci (Colch) PG - 1-2 SB - M CY - ENGLAND IP - 1 VI - 88 JC - DIZ EM - 9507 AD - Department of Physiology, Humboldt University-Charite, Berlin, Germany. RF - 16 CM - Comment on: Clin Sci (Colch) 1995 Jan;88(1):103-9 PMID- 7704990 SO - Clin Sci (Colch) 1995 Jan;88(1):1-2 UI - 95346759 AU - Stauss HM AU - Zhu YC AU - Redlich T AU - Adamiak D AU - Mott A AU - Kregel KC AU - Unger T TI - Angiotensin-converting enzyme inhibition in infarct-induced heart failure in rats: bradykinin versus angiotensin II. LA - Eng MH - Adrenergic beta-Antagonists/pharmacology/therapeutic use MH - Analysis of Variance MH - Angiotensin II/*antagonists & inhibitors MH - Angiotensin-Converting Enzyme Inhibitors/pharmacology/*therapeutic use MH - Animal MH - Biphenyl Compounds/pharmacology/therapeutic use MH - Bradykinin/analogs & derivatives/*antagonists & inhibitors/pharmacology/therapeutic use MH - Comparative Study MH - Disease Models, Animal MH - Heart/physiology MH - Heart Failure, Congestive/*drug therapy/mortality/pathology MH - Hemodynamics/drug effects/physiology MH - Imidazoles/pharmacology/therapeutic use MH - Isoquinolines/pharmacology/therapeutic use MH - Male MH - Myocardial Contraction/drug effects MH - Myocardial Infarction/*drug therapy/mortality/pathology MH - Myocardium/pathology MH - Organ Weight MH - Rats MH - Rats, Wistar MH - Tetrazoles/pharmacology/therapeutic use RN - 0 (Adrenergic beta-Antagonists) RN - 0 (Angiotensin-Converting Enzyme Inhibitors) RN - 0 (Biphenyl Compounds) RN - 0 (Imidazoles) RN - 0 (Isoquinolines) RN - 0 (Tetrazoles) RN - 103775-10-6 (moexipril) RN - 11128-99-7 (Angiotensin II) RN - 114798-26-4 (losartan) RN - 130308-48-4 (icatibant) RN - 58-82-2 (Bradykinin) PT - JOURNAL ARTICLE DA - 950829 DP - 1994 Oct IS - 1350-6277 TA - J Cardiovasc Risk PG - 255-62 SB - M CY - ENGLAND IP - 3 VI - 1 JC - CE7 AA - Author EM - 9511 AB - BACKGROUND: The beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in the prevention of heart failure following myocardial infarction are widely accepted. However, the underlying mechanisms are still a matter of discussion. We therefore investigated the relative contribution of the breakdown of bradykinin and of the inhibition of angiotensin-II synthesis to the beneficial actions of ACE inhibitors in chronic heart failure following myocardial infarction. METHODS: We compared the effects pretreatment with the ACE inhibitor moexipril with those of the type 1 angiotensin (AT1)-receptor antagonist losartan on structural and functional cardiac parameters after myocardial infarction in rats. In addition, the bradykinin B2- receptor antagonist icatabant was used to investigate the role of bradykinin in the cardioprotective effects of ACE inhibition. Rats underwent a sham operation or surgery to induce myocardial infarction. Treatment was started 1 week before myocardial infarction and continued for another 6 weeks after the procedure. RESULTS: Moexipril reduced infarct size (100 +/- 9mm2 compared with 165 +/- 8mm2), the ratio of total heart weight to body weight (2.6 +/- 0.1 g/kg compared with 2.9 +/- 0.1 g/kg) and end-diastolic pressure (8.2 +/- 1.5 mmHg compared with 14.0 +/- 1.7 mmHg). All of these effects of the ACE inhibitor were blocked by concomitant treatment with icatibant. Losartan did not affect any of these cardiac parameters. CONCLUSION: The cardioprotective effects of the ACE inhibitor moexipril administered before myocardial infarction in the present study were a result of the reduced breakdown of kinins rather than of the reduced synthesis of angiotensin II. AD - Department of Pharmacology, University of Heidelberg, Germany. PMID- 7621306 SO - J Cardiovasc Risk 1994 Oct;1(3):255-62 UI - 94295836 AU - Kregel KC AU - Stauss H AU - Unger T TI - Modulation of autonomic nervous system adjustments to heat stress by central ANG II receptor antagonism. LA - Eng MH - Angiotensin II/pharmacology MH - Animal MH - Argipressin/blood MH - Autonomic Nervous System/*physiopathology MH - Biphenyl Compounds/pharmacology MH - Blood Pressure/drug effects MH - Body Temperature MH - Brain/*metabolism MH - Heart Rate/drug effects MH - *Heat MH - Imidazoles/pharmacology MH - Injections, Intraventricular MH - Male MH - Rats MH - Rats, Wistar MH - Receptors, Angiotensin/*antagonists & inhibitors MH - Stress/*physiopathology MH - Support, Non-U.S. Gov't MH - Support, U.S. Gov't, P.H.S. MH - Tetrazoles/pharmacology MH - Viscera/innervation RN - 0 (Biphenyl Compounds) RN - 0 (Imidazoles) RN - 0 (Receptors, Angiotensin) RN - 0 (Tetrazoles) RN - 11128-99-7 (Angiotensin II) RN - 113-79-1 (Argipressin) RN - 114798-26-4 (losartan) PT - JOURNAL ARTICLE ID - AG-12350/AG/NIA DA - 940802 DP - 1994 Jun IS - 0002-9513 TA - Am J Physiol PG - R1985-91 SB - M CY - UNITED STATES IP - 6 Pt 2 VI - 266 JC - 3U8 AA - Author EM - 9410 AB - The purpose of this study was to determine whether central angiotensin II (ANG II) participates in mediating selected sympathetic nervous system and neuroendocrine adjustments to heat stress in conscious freely moving rats. Mean arterial pressure (MAP), heart rate (HR), splanchnic sympathetic nerve activity (SpNA), plasma arginine vasopressin (AVP) concentration, and colonic temperature were measured before and during whole body heating (42 degrees C ambient temperature). Heating was stopped when a colonic temperature of 41 degrees C was attained. On consecutive days, rats received an intracerebroventricular (icv) injection of saline (0.9%) or 25 micrograms of the ANG II AT1-selective receptor antagonist losartan 20 min before the start of heating. Neither treatment influenced control levels of any parameter. The increase above baseline for MAP at the end of heating was attenuated by > 50% in the losartan, compared with the saline trial (P < 0.05), while HR remained unchanged from control values for both trials. Pretreatment with losartan icv eliminated the increase in SpNA observed during the heating period in the saline trial. Furthermore, the magnitude of change in plasma AVP during heating was significantly elevated in rats after icv administration of saline compared with losartan. These findings indicate that central ANG II receptor antagonism significantly attenuates the heating-induced elevations in MAP, sympathetic neural activity to visceral regions, and plasma AVP and suggest that the central nervous system actions of endogenous ANG II are required for full expression of the sympathoexcitatory, pressor, and neuroendocrine responses associated with nonexertional heat stress in the conscious rat. AD - Department of Exercise and Sport Sciences, University of Arizona, Tucson 85721. PMID- 8024055 SO - Am J Physiol 1994 Jun;266(6 Pt 2):R1985-91 UI - 93072427 AU - Persson PB AU - Stauss H AU - Chung O AU - Wittmann U AU - Unger T TI - Spectrum analysis of sympathetic nerve activity and blood pressure in conscious rats. LA - Eng MH - Animal MH - *Blood Pressure/drug effects MH - Comparative Study MH - Electrophysiology/methods MH - Oscillometry MH - Parasympatholytics/pharmacology MH - Rats MH - Rats, Inbred SHR MH - Rats, Inbred WKY MH - Support, Non-U.S. Gov't MH - Sympathetic Nervous System/*physiology MH - Sympatholytics/pharmacology RN - 0 (Parasympatholytics) RN - 0 (Sympatholytics) PT - JOURNAL ARTICLE DA - 921222 DP - 1992 Nov IS - 0002-9513 TA - Am J Physiol PG - H1348-55 SB - M CY - UNITED STATES IP - 5 Pt 2 VI - 263 JC - 3U8 AA - Author EM - 9302 AB - This study tests whether the power spectrum of blood pressure (BP) provides information toward the sympathovagal balance of BP control by comparing the BP (femoral arterial catheter) spectrum with the spectrum of the efferent sympathetic nerve activity (SNA, bipolar electrode around splanchnic nerve). A remarkable resemblance between both spectra was found. A high-frequency component (HF) linked to respiration and a slower fluctuation type between 0.15 and 0.6 Hz (LF) were identified. There was a large and significant coherence only in the HF range of the BP and SNA power spectrum (P < 0.01). The phase lag of SNA and BP was roughly 200 ms. The recordings were repeated during pharmacological blockade in nine Wistar-Kyoto rats (WKY) and nine spontaneously hypertensive rats (SHR). alpha 1-Adrenoceptor blockade (prazosin) reduced the proportional LF power of BP in both rat strains (WKY P < 0.01, SHR P < 0.05) in favor of HF (WKY P < 0.01, SHR P < 0.01). Parasympathetic blockade (methylscopolamine) had no effect on proportions of power. Similarly, there were no significant differences in the proportional HF and LF power spectra of WKY and SHR. These data provide direct evidence for a relationship between the BP and SNA power spectra; however, only the acute changes in the sympathetic tone changed the LF-HF relationship. AD - I. Physiologisches Institut, Ruprecht-Karls Universitat, Heidelberg, Germany. PMID- 1443189 SO - Am J Physiol 1992 Nov;263(5 Pt 2):H1348-55 UI - 92290986 AU - Fletcher EC AU - Lesske J AU - Behm R AU - Miller CC 3d AU - Stauss H AU - Unger T TI - Carotid chemoreceptors, systemic blood pressure, and chronic episodic hypoxia mimicking sleep apnea. LA - Eng MH - Animal MH - Anoxia/*physiopathology MH - Blood Pressure/physiology MH - Carotid Body/physiopathology MH - Chemoreceptors/physiopathology MH - Comparative Study MH - Denervation MH - Disease Models, Animal MH - Male MH - Rats MH - Rats, Inbred Strains MH - Sleep Apnea Syndromes/*physiopathology MH - Support, U.S. Gov't, Non-P.H.S. PT - JOURNAL ARTICLE DA - 920713 DP - 1992 May IS - 8750-7587 TA - J Appl Physiol PG - 1978-84 SB - M CY - UNITED STATES IP - 5 VI - 72 JC - HEG AA - Author EM - 9209 AB - We have described a rat model that responds to repetitive episodic hypoxia (12-s infusions of nitrogen into daytime sleeping chambers every 30 s, 7 h/day for 35 days) with an increase in diurnal systemic blood pressure. We hypothesized that afferent information from the peripheral chemoreceptors may be necessary to produce diurnal blood pressure elevation in this hypoxia model. Carotid body denervation (CBD) was accomplished by severing both carotid sinus nerves in two groups of male Wistar rats (250-375 g). Group 4 CBD rats were subjected to intermittent hypoxia for 35 days (3-5% nadir ambient O2) as described above, whereas group 5 CBD rats remained unhandled in their usual cages. Additional sham-operated controls included group 2 sham- "hypoxia" rats, which were housed in chambers identical to the hypoxia rats but supplied with compressed air instead of nitrogen, group 1 (not denervated) rats, which remained unhandled in their usual cages, and group 3 sham-operated rats, which were subjected to 35 days of intermittent hypoxia identical to group 4 CBD rats. Femoral arterial baseline and end-of-study blood pressures were measured in conscious rats. The group 3 rats exposed to episodic hypoxia displayed a 13-mmHg increase in mean blood pressure, whereas the other groups showed no significant change from baseline. Left ventricular hypertrophy was evident in all rats exposed to episodic hypoxia, but right ventricular hypertrophy was evident only in the group 4 rats. All CBD rats developed increased hematocrit and hemoglobin, while the group 3 rats (non-CBD, episodic hypoxia) did not. The baroreceptor reflex at baseline was not depressed in the CBD rats.(ABSTRACT TRUNCATED AT 250 WORDS) AD - Department of Pharmacology, Ruprecht-Karls University, Heidelberg, Federal Republic of Germany. PMID- 1601808 SO - J Appl Physiol 1992 May;72(5):1978-84 UI - 92174452 AU - Rettig R AU - Folberth CG AU - Graf C AU - Kopf D AU - Stauss H AU - Unger T TI - Post-transplantation hypertension in recipients of renal grafts from hypertensive donor rats. LA - Eng MH - Animal MH - Antihypertensive Agents/therapeutic use MH - Hypertension/*etiology/genetics/prevention & control MH - Hypertension, Renovascular/etiology MH - *Kidney Transplantation MH - Male MH - Rats MH - Rats, Inbred SHR MH - Rats, Inbred WKY MH - *Tissue Donors RN - 0 (Antihypertensive Agents) PT - JOURNAL ARTICLE DA - 920409 DP - 1991 Dec IS - 0147-958X TA - Clin Invest Med PG - 492-8 SB - M CY - CANADA IP - 6 VI - 14 JC - DFG AA - Author EM - 9206 AB - Renal transplantations were performed using stroke-prone spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) as kidney donors and bilaterally nephrectomized F1 hybrids, bred from SHR x WKY parents as renal graft recipients. Recipients of renal grafts from adult, naive SHR but not from adult normotensive WKY kidney donors developed post- transplantation hypertension. Permanent blood pressure normalization by antihypertensive treatment in adult SHR kidney donors, as well as the young, prehypertensive age of SHR kidney donors reduced but did not prevent the development of post-transplantation hypertension. Increasing renal perfusion pressure in WKY kidney donors (chronic 2- kidney 1-clip renovascular hypertension) also resulted in post- transplantation hypertension in recipients of the non-clipped kidneys. Blood pressure remained normal in recipients of renal grafts from young WKY kidney donors. These data suggest that SHR kidneys carry a genetic defect which can give rise to post-transplantation hypertension and which therefore may also play a role in the development of hypertension in naive SHR. In addition, secondary hypertension-induced renal damage may also contribute to post-transplantation hypertension in recipients of renal grafts from hypertensive donors. AD - Department of Pharmacology, University of Heidelberg, Germany. PMID- 1794203 SO - Clin Invest Med 1991 Dec;14(6):492-8 UI - 92092614 AU - Rettig R AU - Folberth CG AU - Graf C AU - Kopf D AU - Stauss H AU - Unger T TI - Are renal mechanisms involved in primary hypertension? Evidence from kidney transplantation studies in rats. LA - Eng MH - Animal MH - Hybridization/genetics/physiology MH - Hypertension/genetics/*physiopathology MH - Hypertension, Renal/*physiopathology MH - Hypertension, Renovascular/physiopathology MH - Kidney Transplantation/*physiology MH - Muscle, Smooth, Vascular/physiopathology MH - Rats MH - Rats, Inbred SHR MH - Rats, Inbred WKY PT - JOURNAL ARTICLE DA - 920127 DP - 1991 Sep 3 IS - 0023-2173 TA - Klin Wochenschr PG - 597-602 SB - M CY - GERMANY IP - 13 VI - 69 JC - KWH AA - Author EM - 9204 AB - Previous renal transplantation experiments in genetically hypertensive and normotensive rat strains indicated that a genetic defect in the kidney may be primarily involved in the pathogenesis of primary hypertension. In order to investigate whether this is also true for the most widely used animal model of primary hypertension, the spontaneously hypertensive rat (SHR), we performed renal transplantations using SHR and normotensive Wistar-Kyoto rats (WKY) as kidney donors and bilaterally nephrectomized F1 hybrids, bred from SHR x WKY parents as renal graft recipients. Our studies were also designed to differentiate between primary and secondary renal mechanisms as a possible cause of posttransplantation hypertension. Recipients of renal grafts from adult, naive SHR but not from adult normotensive WKY kidney donors developed posttransplantation hypertension. Permanent blood pressure normalization by antihypertensive treatment in adult SHR kidney donors and prehypertensive, young age of SHR kidney donors reduced, but did not prevent, posttransplantation hypertension. Increasing renal perfusion pressure in WKY kidney donors (2-kidney 1- clip hypertension) also resulted in posttransplantation hypertension in recipients of the non-clipped kidneys. Blood pressure remained normal in recipients of renal grafts from young WKY kidney donors. These data suggest that SHR kidneys carry a genetic defect which may be primarily involved in the pathogenesis of primary hypertension. AD - Pharmakologisches Institut, Universitat Heidelberg. PMID- 1753682 SO - Klin Wochenschr 1991 Sep 3;69(13):597-602 UI - 92120183 AU - Bao G AU - Qadri F AU - Stauss B AU - Stauss H AU - Gohlke P AU - Unger T TI - HOE 140, a new highly potent and long-acting bradykinin antagonist in conscious rats. LA - Eng MH - Amino Acid Sequence MH - Animal MH - Bradykinin/analogs & derivatives/administration & dosage/*antagonists & inhibitors/pharmacology/pharmacokinetics MH - Catecholamines/blood MH - Comparative Study MH - Half-Life MH - Male MH - Molecular Sequence Data MH - Oligopeptides/*pharmacology/pharmacokinetics MH - Rats MH - Rats, Inbred Strains RN - 0 (Catecholamines) RN - 0 (Oligopeptides) RN - 103433-42-7 (B 4146) RN - 130308-48-4 (icatibant) RN - 58-82-2 (Bradykinin) PT - JOURNAL ARTICLE DA - 920225 DP - 1991 Jul 23 IS - 0014-2999 TA - Eur J Pharmacol PG - 179-82 SB - M CY - NETHERLANDS IP - 1 VI - 200 JC - EN6 AA - Author EM - 9204 AB - The inhibitory effects of the new bradykinin antagonist HOE 140 (D-Arg- Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg) on depressor responses to exogenous bradykinin were investigated in conscious rats and compared with those of the bradykinin antagonist B4146 (D-Arg-Hyp-Pro-Gly-Thi- Ser-D-Pro-Thi-Arg). HOE 140 showed a 250-700-fold higher potency in vivo and a much longer biological half-life than B4146. Plasma catecholamines were not increased after application of HOE 140, indicating that this compound did not interfere with catecholamine release. HOE 140 proved to be a highly potent, specific and long-acting bradykinin B2-receptor antagonist. AD - Department of Pharmacology, University of Heidelberg, F.R.G. PMID- 1769370 CU - 95 SO - Eur J Pharmacol 1991 Jul 23;200(1):179-82 UI - 90202047 AU - Rettig R AU - Folberth CG AU - Stauss H AU - Kopf D AU - Waldherr R AU - Baldauf G AU - Unger T TI - Hypertension in rats induced by renal grafts from renovascular hypertensive donors. LA - Eng MH - Animal MH - Blood Pressure MH - Drinking MH - Glomerular Filtration Rate MH - Hybridization MH - Hypertension/*etiology/physiopathology MH - Hypertension, Renovascular/*physiopathology MH - Kidney/pathology/*physiopathology/radiography MH - *Kidney Transplantation MH - Male MH - Rats MH - Rats, Inbred SHR MH - Rats, Inbred WKY MH - *Tissue Donors MH - Urea/blood MH - Urography RN - 57-13-6 (Urea) PT - JOURNAL ARTICLE DA - 900509 DP - 1990 Apr IS - 0194-911X TA - Hypertension PG - 429-35 SB - M CY - UNITED STATES IP - 4 VI - 15 JC - GK7 AA - Author EM - 9007 AB - Renal transplantations were performed, using microsurgical techniques, with adult male two-kidney, one clip hypertensive rats (n = 9) and sham- operated normotensive Wistar-Kyoto rats (n = 8) as kidney donors and with F1 hybrids, bred from Wistar-Kyoto and stroke-prone spontaneously hypertensive rat parents, as recipients. Systolic blood pressure before surgery was 200 +/- 2.7 mm Hg in hypertensive and 115 +/- 1.7 mm Hg in normotensive donors and 144 +/- 7.1 and 138 +/- 3.5 mm Hg in the two groups of recipients. Renal hypertension in donors was maintained for 14 weeks before surgery was performed and the nonischemic kidneys were transplanted. Bilaterally nephrectomized recipients of renal grafts from hypertensive donors developed sustained hypertension (185 +/- 3.9 mm Hg). In contrast, in recipients of renal grafts from normotensive donors, blood pressure decreased significantly to the level of the donors (111 +/- 3.7 mm Hg). Posttransplantation hypertension in recipients of renal grafts from hypertensive donors was associated with intrarenal vascular hypertrophy, smaller kidneys, a decreased glomerular filtration rate, an increased plasma urea concentration, and polydipsia as compared with normotensive transplanted controls. Renal pyelograms revealed no gross anatomic alterations of transplanted kidneys. Our data indicate that secondary damage to the renal grafts caused by high perfusion pressure before transplantation can induce hypertension in recipients of these kidneys. Furthermore, our data suggest that renal mechanisms may be necessary to maintain borderline hypertension in F1 hybrids. AD - Department of Pharmacology, German Institute for Hypertension Research, University of Heidelberg, FRG. PMID- 2318524 CU - 90 SO - Hypertension 1990 Apr;15(4):429-35 UI - 90196268 AU - Rettig R AU - Folberth C AU - Stauss H AU - Kopf D AU - Waldherr R AU - Unger T TI - Role of the kidney in primary hypertension: a renal transplantation study in rats. LA - Eng MH - Animal MH - Antihypertensive Agents/pharmacology MH - Bicyclo Compounds/pharmacology MH - Blood Pressure/drug effects MH - Drinking MH - Hypertension/pathology/*physiopathology MH - Kidney/pathology/*physiopathology MH - *Kidney Transplantation MH - Kidney Tubules/pathology MH - Male MH - Organ Weight MH - Rats MH - Rats, Inbred SHR MH - Rats, Inbred WKY RN - 0 (Antihypertensive Agents) RN - 0 (Bicyclo Compounds) RN - 87333-19-5 (Ramipril) PT - JOURNAL ARTICLE DA - 900423 DP - 1990 Mar IS - 0002-9513 TA - Am J Physiol PG - F606-11 SB - M CY - UNITED STATES IP - 3 Pt 2 VI - 258 JC - 3U8 AA - Author EM - 9006 AB - We have previously shown that transplantation of kidneys from genetically hypertensive to normotensive rats result in hypertension in renal graft recipients. To investigate whether this posttransplantation hypertension may have been the result of damage to the renal graft by high perfusion pressure before transplantation, we normalized blood pressure throughout life in spontaneously hypertensive rat (SHR) kidney donors by continuous antihypertensive treatment with the angiotensin- converting enzyme inhibitor ramipril (1 mg.kg-1.day-1 in drinking fluid). When kidneys from these rats were transplanted at age 20 wk to age-matched bilaterally nephrectomized F1 hybrids bred from SHR and Wistar-Kyoto (WKY) parents, posttransplantation hypertension still developed. In contrast, blood pressure did not change significantly in recipients of kidneys from ramipril-treated WKY rats. In the initial phase, recipients of SHR kidneys had a lower body weight and higher plasma urea concentrations than recipients of WKY kidneys. However, in the chronic phase, there were no significant differences between the two groups with respect to daily water intake, plasma urea concentration, glomerular filtration rate, renal blood flow, and weight of transplanted kidneys; no histological differences were observed between renal grafts from WKY and SHR donors, except for structural vascular hypertrophy in the latter group. We conclude that posttransplantation hypertension in recipients of SHR kidney grafts also develops, when the grafts have not been subjected to high renal perfusion pressure before transplantation. Our data support the hypothesis that SHR kidneys carry a primary defect, which can induce hypertension in renal graft recipients. AD - Department of Pharmacology, University of Heidelberg, Federal Republic of Germany. PMID- 2138422 CU - 92 SO - Am J Physiol 1990 Mar;258(3 Pt 2):F606-11 UI - 91059488 AU - Rettig R AU - Folberth C AU - Kopf D AU - Stauss H AU - Unger T TI - Role of the kidney in the pathogenesis of primary hypertension. LA - Eng MH - Animal MH - Blood Pressure MH - Body Water/metabolism MH - Electrolytes/metabolism MH - Human MH - Hypertension/etiology/genetics/*physiopathology MH - Kidney/metabolism/*physiology MH - Kidney Transplantation MH - Postoperative Complications MH - Rats MH - Rats, Inbred Strains MH - Rats, Inbred SHR/physiology MH - Rats, Mutant Strains MH - Sodium Chloride/metabolism RN - 0 (Electrolytes) RN - 7647-14-5 (Sodium Chloride) PT - JOURNAL ARTICLE PT - REVIEW PT - REVIEW, TUTORIAL DA - 910109 DP - 1990 IS - 0730-0077 TA - Clin Exp Hypertens [A] PG - 957-1002 SB - M CY - UNITED STATES IP - 6 VI - 12 JC - DCJ AA - Author EM - 9103 AB - Primary hypertension in animals and humans probably represents several different pathophysiological states rather than being a uniform nosological entity. Among other factors, renal mechanisms may be primarily and secondarily involved. The availability of genetically homologous animal models for hypertension has greatly promoted studies on the etiology and pathogenesis of high blood pressure disease. In particular, renal transplantation studies between genetically hypertensive and normotensive rats from three different models have provided strong evidence for a primary role of the kidney in genetic hypertension. Other factors, such as vascular, neural, and humoral mechanisms have also been shown to be involved and may be particularly effective in increasing blood pressure, when they act through the kidney. Several functional and biochemical differences have been identified between kidneys from genetically hypertensive and normotensive animals. However, the relative contribution of each of these factors to the development of primary hypertension remains to be determined. Evidence from studies on human renal graft recipients also indicates that, among other factors, the kidney plays an important role in the development of primary hypertension in humans. AD - Department of Pharmacology, University of Heidelberg, Federal Republic of Germany. RF - 115 PMID- 2245518 CU - 91 SO - Clin Exp Hypertens [A] 1990;12(6):957-1002 UI - 89349423 AU - Rettig R AU - Stauss H AU - Folberth C AU - Ganten D AU - Waldherr B AU - Unger T TI - Hypertension transmitted by kidneys from stroke-prone spontaneously hypertensive rats. LA - Eng MH - Animal MH - *Blood Pressure MH - Cerebrovascular Disorders/etiology/*physiopathology MH - Crosses, Genetic MH - Hypertension, Renovascular/genetics/*physiopathology MH - Kidney/pathology/physiopathology/*transplantation MH - *Kidney Transplantation MH - Male MH - Rats MH - Rats, Inbred SHR MH - Rats, Inbred WKY MH - Renin/blood MH - Urea/blood RN - EC 3.4.23.15 (Renin) RN - 57-13-6 (Urea) PT - JOURNAL ARTICLE DA - 890914 DP - 1989 Aug IS - 0002-9513 TA - Am J Physiol PG - F197-203 SB - M CY - UNITED STATES IP - 2 Pt 2 VI - 257 JC - 3U8 AA - Author EM - 8911 AB - We determined whether transplantations of kidneys from stroke-prone spontaneously hypertensive rats (SPSHR) and from normotensive Wistar- Kyoto rats (WKY) alter blood pressure in renal graft recipients. Kidneys taken from seven male SPSHR and seven male WKY rats (blood pressure 186 +/- 4.8 and 111 +/- 3.7 mmHg, respectively) at the age of 20 wk were transplanted, using microsurgical techniques, to bilaterally nephrectomized age-matched male F1 hybrids (blood pressure 136 +/- 2.6 and 138 +/- 6.3 mmHg, respectively) bred from SPSHR and WKY parents. After renal transplantation, blood pressure in recipients of SPSHR kidneys rose to 146 +/- 11.8 (week 2), 163 +/- 16.4 (week 3), 192 +/- 17.1 (week 4), 222 +/- 17.7 (week 5), 221 +/- 12.6 (week 6), 218 +/- 20.3 (week 7), and 239 +/- 9.2 mmHg (week 8). There was no significant change in blood pressure in recipients of WKY kidneys. All rats recovered rapidly from surgery. After renal transplantation, there was a significant increase in daily water intake, a decrease in plasma renin activity, and a slight rise in plasma urea concentration. Our data show that transplantation of kidneys from adult SPSHR causes hypertension in normotensive recipients, indicating a major function for the kidney in SPSHR hypertension. AD - German Institute for High Blood Pressure Research, University of Heidelberg, Federal Republic of Germany. PMID- 2669526 CU - 90 SO - Am J Physiol 1989 Aug;257(2 Pt 2):F197-203