Vasopressin withdrawal produces hypotension in the spontaneously hypertensive rat

1985 ◽  
Vol 249 (1) ◽  
pp. H193-H197 ◽  
Author(s):  
E. K. Chiu ◽  
J. R. McNeill
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Pressor Agent

In spontaneously hypertensive rats (SHR) and their normotensive Wistar-Kyoto controls (WKY), prolonged intravenous infusions of either arginine vasopressin (AVP, 8 mU X kg-1 X min-1) or phenylephrine (PE, 20 nmol X kg-1 X min-1) resulted in similar rises in arterial pressure. Heart rate fell greatly in the WKY but not in the SHR. Withdrawal of the PE infusion resulted in moderate decreases in blood pressure and increases in heart rate; these responses were similar in SHR and WKY. At 5 h after PE withdrawal, blood pressure and heart rate returned to basal values. In contrast, withdrawal of the AVP infusion was associated with greater falls in blood pressure and rises in heart rate. Blood pressure and heart rate in both the SHR and the WKY at 5 h after AVP were significantly different from their respective basal values. The effects of AVP withdrawal on either blood pressure or heart rate were significantly greater in the SHR than in the WKY. At 5 h after the withdrawal of AVP, blood pressure in the SHR was reduced to normotensive levels. These results suggest that the withdrawal effect was specific to AVP, was more marked in the SHR, and might not result from only the rise in blood pressure seen during the intravenous infusion of the pressor agent.

scholarly journals Duration of Electrically Induced Atrial Fibrillation Is Augmented by High Voltage of Stimulus with Higher Blood Pressure in Hypertensive Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Tomomi Nagayama ◽  
Yoshitaka Hirooka ◽  
Akiko Chishaki ◽  
Masao Takemoto ◽  
Yasushi Mukai ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Blood Pressure ◽  
Arterial Pressure ◽  
High Voltage ◽  
Spontaneously Hypertensive Rats ◽  
Low Voltage ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Stimulus ◽  
Wistar Kyoto

Objective.Many previous clinical studies have suggested that atrial fibrillation (AF) is closely associated with hypertension. However, the benefits of antihypertensive therapy on AF are still inconsistent, and it is necessary to explore the factors augmenting AF in hypertensive rats. The aim of the present study was to investigate the correlation between arterial pressure or voltage stimulus and to the duration of electrically induced AF in normotensive or hypertensive rats.Methods.AF was reproducibly induced by transesophageal atrial burst pacing in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We did the burst pacing at high (20 V) or low (5 V) voltage.Results.Duration of AF did not correlate with systolic blood pressure (SBP) and stimulus voltage in WKY. However, only in SHR, duration of AF with high stimulus voltage significantly correlated with SBP and was significantly longer in high than in low voltage stimulus.Discussion and Conclusion.Duration of AF is augmented by high voltage stimulus with higher blood pressure in SHR.

Regression of myocardial hypertrophy and influence of adrenergic system

1983 ◽  
Vol 244 (1) ◽  
pp. H97-H101 ◽  
Author(s):  
S. Sen ◽  
R. C. Tarazi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Regression Analysis ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Myocardial Hypertrophy ◽  
Cardiac Response ◽  
Adrenergic System ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Studies of regression of myocardial hypertrophy in spontaneously hypertensive rats (SHR) suggest that the adrenergic system may play an important role in the reversal of hypertrophy. The effect of propranolol on reversal of hypertrophy, however, is still controversial. This study describes the effect of propranolol, given alone or in combination with hydralazine in different ratios for 4 wk, on blood pressure (BP), ventricular weight, and myocardial catecholamine (MC) concentrations. The data show that a certain ratio of propranolol to hydralazine (750:30) leads to moderate BP control (196-156 mmHg) without increased MC (634 vs. 552 ng/g) and moderately reduced hypertrophy. Reduction of BP alone with increased MC (hydralazine alone) or reduction of MC without BP control (propranolol alone) failed to reduce hypertrophy. A significant correlation between both ventricular weight and heart rate with MC (r = 0.6) was obtained by multiple regression analysis. This study suggests that adrenergic factors seem to play an important role in modulating structural cardiac response to variations in arterial pressure.

Clonidine fails to reduce pressor responsiveness of conscious spontaneously hypertensive rats to vasopressin

1986 ◽  
Vol 64 (3) ◽  
pp. 284-289 ◽  
Author(s):  
Sunil Datar ◽  
William H. Laverty ◽  
J. Robert McNeill
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Reflex Activity ◽  
Unexpected Finding ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto ◽  
Shr And Wky Rats

Pressor responses and heart rate responses to intravenous injections (3.5–50.0 pmol/kg) of arginine vasopressin (AVP) were recorded in saline- and clonidine-treated spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Clonidine (20 μg/kg, i. v.) caused a marked fall of arterial pressure in SHR but not in WKY rats so that, 20 min after the injection of the α2-adrenoceptor agonist, arterial pressure was similar in the two strains of rats. The curve expressing the relationship between the dose of AVP and the increase of arterial pressure for saline-treated SHR was positioned to the left of that for saline-treated WKY rats. This enhanced pressor responsiveness of SHR to AVP may have been related to impaired reflex activity since heart rate fell much less in SHR than in WKY rats for a given elevation in pressure. Pressure responses to AVP were augmented by clonidine in both SHR and WKY rats so that, similar to saline-treated rats, pressor responsiveness to the peptide was still greater in SHR. Heart rate responses to AVP were not altered significantly by clonidine. The results indicate that clonidine fails to enhance reflex activity and reduce pressor responsiveness of SHR to AVP. The increased pressor responsiveness of both SHR and WKY rats to AVP following clonidine was an unexpected finding and may be related to a peripheral interaction between α-adrenergic agonists and AVP.

Relationship between baroreceptor reflex function and end-organ damage in spontaneously hypertensive rats

1999 ◽  
Vol 277 (3) ◽  
pp. H1200-H1206 ◽  
Author(s):  
Zheng-Zheng Shan ◽  
Sheng-Ming Dai ◽  
Ding-Feng Su
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Spontaneously Hypertensive Rats ◽  
Organ Damage ◽  
Baroreceptor Reflex ◽  
Hypertensive Rats ◽  
Baroreceptor Sensitivity ◽  
Spontaneously Hypertensive ◽  
End Organ Damage ◽  
Wistar Kyoto

The purpose of this study was to further illustrate the relationship between baroreceptor reflex sensitivity (BRS) and hypertensive end-organ damage (EOD) and to test the hypothesis that impairment of BRS aggravates EOD in hypertension. We studied baroreflex-mediated changes in heart rate [expressed as baroreceptor sensitivity to heart rate control (BRSHR)] and blood pressure [expressed as baroreceptor sensitivity to blood pressure control (BRSBP)] in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) that were used as controls, both at the age of 50–52 wk. Rats were also instrumented to record BP, HR, and BP variability (BPV) in the conscious, unrestrained state. In SHR compared with WKY, BP and BPV were significantly increased, whereas BRSHR and BRSBP were significantly decreased. SHR had remarkable EOD when compared with WKY (EOD score: 6.3 ± 2.5 vs. 2.9 ± 0.8, P < 0.01). Univariate regressive analysis demonstrated that EOD score was increased with BP and BPV and decreased with BRS. In multivariate analysis, EOD score was predicted by greater systolic BP and lower BRS and HR variability. These results indicate that BRS is negatively related to BPV and EOD score, and impaired BRS might be one of the major causes for hypertensive EOD.

Cell Membrane Microviscosity and Ca2+-Mg2+-ATPase Activity do Not Contribute to Hypertension in the Spontaneously Hypertensive Rat Model

1993 ◽  
Vol 85 (5) ◽  
pp. 585-591 ◽  
Author(s):  
Robert I Norman ◽  
Navtej Achall
Keyword(s):  
Blood Pressure ◽  
Atpase Activity ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Membrane Microviscosity ◽  
Spontaneously Hypertensive ◽  
Blood Pressures ◽  
Wistar Kyoto ◽  
Spontaneously Hypertensive Rat Model

1. The relationships between systolic blood pressure and altered erythrocyte Ca2+-Mg2+-ATPase activity and membrane microviscosity were assessed in membranes prepared from 20-week-old female Wistar-Kyoto normotensive and spontaneously hypertensive rats obtained from two different sources (Charles River and Harlan OLAC) and a second filial (F2) generation derived from a cross between Wistar-Kyoto rats and spontaneously hypertensive rats from one source (Charles River). 2. Spontaneously hypertensive rats from both sources had systolic blood pressures significantly higher than those of Wistar-Kyoto animals (P <0.05; 151 + 4 and 110 + 3 mmHg, Charles River; 155 + 4 and 122 + 4 mmHg, Harlan OLAC). The systolic blood pressures for the F2 rat population ranged between 73 and 168 mmHg. 3. Ca2+-Mg2+-ATPase activity was measured as ATP-dependent 45Ca2+ uptake into inside-out vesicles and microviscosity assessed by the measurement of polarization anisotropy of membrane incorporated fluorescent probes including 1,6-diphenyl-1,3,5-hexatriene, trimethylamino-1,6-diphenyl-1,3,5-hexatriene and a series of anthroyloxy fatty acids. 4. Contrary to previous studies, no relationship between adult systolic blood pressure and erythrocyte Ca2+-Mg2+-ATPase activity or general or localized membrane microviscosity was indicated by the comparison of spontaneously hypertensive and Wistar-Kyoto animals or in the analysis of the F2 rat population. 5. These results suggest that Ca2+-Mg2+-ATPase activity and membrane microviscosity are causally unrelated to hypertension in these animals. On the assumption that biophysical properties of the erythrocyte membrane reflect those of smooth muscle, our results suggest that membrane alteration does not play a significant role in the pathogenesis of hypertension in the spontaneously hypertensive rat model.

Blood Pressure and Heart Rate Responses to Centrally Administered Substance P Are Increased in Spontaneously Hypertensive Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 299s-302s ◽  
Author(s):  
T. Unger ◽  
R. W. Rockhold ◽  
T. Yukimura ◽  
R. Rettig ◽  
D. Ganten
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Substance P ◽  
Spontaneously Hypertensive Rats ◽  
Similar Degree ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Intracerebroventricular Injections ◽  
Wistar Kyoto

1. The cardiovascular effects after intracerebroventricular injections of substance P were investigated in normotensive Wistar-Kyoto and in spontaneously hypertensive rats. 2. Substance P increased blood pressure in both rat strains. Wistar-Kyoto rats responded with moderate, dose-dependent blood pressure increases, and heart rate decreased; spontaneously hypertensive rats showed two- to three-fold increased pressor effects and, concomitantly, marked heart rate increases to intracerebroventricular injections of substance P. 3. Sino-aortic baroreceptor denervation rendered Wistar-Kyoto rats supersensitive to intracerebroventricular substance P to a similar degree as unoperated spontaneously hypertensive rats. Sino-aortic denervation had no effect on the blood pressure responses to the peptide in spontaneously hypertensive rats. 4. The central pressor actions of substance P could be markedly attenuated. by intracerebroventricular pretreatment with the derivative of γ-aminobutyric acid, baclofen. 5. We conclude that the baroreceptor reflex is disturbed in spontaneously hypertensive rats. Substance P may contribute to the pathogenesis of hypertension. The effector pathways appear to be different from angiotensin.

Insulin sensitivity and hemodynamic responses to insulin in Wistar-Kyoto and spontaneously hypertensive rats

1996 ◽  
Vol 271 (4) ◽  
pp. E658-E668 ◽  
Author(s):  
M. Pitre ◽  
A. Nadeau ◽  
H. Bachelard
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Insulin Sensitivity ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Hemodynamic Responses ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Vascular Beds ◽  
Wistar Kyoto

The insulin-mediated vasodilator effect has been proposed as an important physiological determinant of insulin action on glucose disposal in normotensive humans. The present study was designed to further examine the acute regional hemodynamic effects of insulin in different vascular beds and to explore the relationships between insulin vascular effects and insulin sensitivity during euglycemic hyperinsulinemic clamps in conscious normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The rats were instrumented with intravascular catheters and pulsed Doppler flow probes to measure blood pressure, heart rate, and regional blood flows. In WKY rats, the euglycemic infusion of insulin (4 and 16 mU.kg-1.min-1) causes vasodilations in renal and hindquarter vascular beds but no changes in mean blood pressure, heart rate, or superior mesenteric vascular conductance. In contrast, in SHR, the same doses of insulin produce vasoconstrictions in superior mesenteric and hindquarter vascular beds and, at high doses, increase blood pressure. Moreover, at the lower dose of insulin tested, we found a reduction in the insulin sensitivity index in the SHR compared with the WKY rats. The present findings provide further evidence for an association between insulin sensitivity and insulin-mediated hemodynamic responses.

Contribution of Vasopressin to the maintenance of blood pressure in deoxycorticosterone-salt induced malignant hypertension in spontaneously hypertensive rats

1986 ◽  
Vol 70 (2) ◽  
pp. 191-198 ◽  
Author(s):  
Masao Hiwatari ◽  
Josephine M. Abrahams ◽  
Takao Saito ◽  
Colin I. Johnston
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Left Ventricular ◽  
Malignant Hypertension ◽  
Minor Importance ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

1. In the present study, deoxycorticosterone (DOC) and salt was administered to Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) by using silicone-rubber implants (DOC acetate, 100 mg/kg) and 0.9% NaCl as drinking water. SHR treated with DOC-salt for 4 weeks showed the characteristics of malignant hypertension including marked increases in blood pressure and left ventricular weight with typical histological changes in the kidney. 2. DOC-salt treatment increased plasma vasopressin levels in WKY (from 6.1 ± 0.5 to 8.9 ± 0.8 pmol/l) but significantly more in SHR (from 5.0 ± 0.6 to 15.8 ±1.2 pmol/l). 3. Intravenous administration of the specific antagonist to the pressor effect of vasopressin, d(CH2)5Tyr(Me)AVP (10μg/kg), decreased mean arterial pressure of DOC-salt treated WKY and SHR by 6.6 ± 0.9mmHg (P < 0.05) and 9.7 ± 1.7 mmHg (P < 0.05) respectively. 4. DOC-water treatment also increased plasma AVP levels in SHR to 10.5 ± 0.8 pmol/l, but the vasopressin antagonist had little effect on blood pressure in these rats. 5. Plasma levels of vasopressin were significantly correlated with both mean arterial pressure (r = 0.64) and left ventricular weight (r = 0.74). This suggests a close relationship between plasma AVP and severity of hypertension. 6. The results of the present experiment demonstrate that vasopressin is part of the overall pressor mechanism which contributes to the maintenance of blood pressure in DOC-salt induced malignant hypertension in SHR, but the small fall in pressure produced by the AVP antagonists suggests that the contribution is of only minor importance.

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