Enhanced diurnal variation of blood pressure in the renal hypertensive rat: effect of angiotensin II suppression

1987 ◽  
Vol 73 (3) ◽  
pp. 271-275 ◽  
Author(s):  
E. C. H. Wallace ◽  
A. J. Balmforth ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Diurnal Rhythm ◽  
Blood Pressure Variability ◽  
Renal Hypertension ◽  
Hypertensive Rats ◽  
Computer Data ◽  
Renal Hypertensive Rat ◽  
Collecting System

1. Chronic two-kidney, one-clip hypertensive rats were infused with captopril for 5 days and the daily variability of blood pressure compared with that for both hypertensive rats infused with glucose and normotensive animals. 2. Blood pressure was measured continuously using a computer data collecting system. 3. Normotensive animals showed a stable level of arterial pressure throughout each 24 h period with troughs occurring when they slept during the daytime. 4. Hypertensive animals given glucose had an enhanced diurnal rhythm of blood pressure compared with normotensive rats, with peaks occurring during periods of activity at night as well as troughs when they slept during the day. 5. Hypertensive rats given captopril retained this enhanced pressure variability, in spite of the fact that blood pressure was significantly lower and angiotensin II was suppressed. 6. These results suggest that angiotensin II is not involved in the increased blood pressure variability of renal hypertension and that some other irreversible mechanism is responsible.

scholarly journals Brain Angiotensin II Type 1 Receptor Blockade Improves Dairy Blood Pressure Variability via Sympathoinhibition in Hypertensive Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-7
Author(s):  
Takuya Kishi ◽  
Yoshitaka Hirooka ◽  
Kenji Sunagawa
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cardiovascular Events ◽  
Blood Pressure Variability ◽  
Active Phase ◽  
Early Morning ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Intracerebroventricular Infusion

Abnormal blood pressure (BP) elevation in early morning is known to cause cardiovascular events. Previous studies have suggested that one of the reasons in abnormal dairy BP variability is sympathoexcitation. We have demonstrated that brain angiotensin II type 1 receptor (AT1R) causes sympathoexcitation. The aim of the present study was to investigate whether central AT1R blockade attenuates the excess BP elevation in rest-to-active phase in hypertensive rats or not. Stroke-prone spontaneously hypertensive rats (SHRSP) were treated with intracerebroventricular infusion (ICV) of AT1R receptor blocker (ARB), oral administration of hydralazine (HYD), or ICV of vehicle (VEH). Telemetric averaged mean BP (MBP) was measured at early morning (EM), after morning (AM), and night (NT). At EM, MBP was significantly lower in ARB to a greater extent than in HYD compared to VEH, though MBP at AM was the same in ARB and HYD. At NT, MBP was also significantly lower in ARB than in HYD. These results in MBP were compatible to those in sympathoexcitation and suggest that central AT1R blockade attenuates excess BP elevation in early active phase and continuous BP elevation during rest phase independent of depressor response in hypertensive rats.

Evidence against an increase in circulating pressor material in renal hypertensive rats

1960 ◽  
Vol 198 (6) ◽  
pp. 1148-1152 ◽  
Author(s):  
Pedro Blaquier ◽  
David F. Bohr ◽  
Sibley W. Hoobler
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Test Animal ◽  
Renal Pedicle ◽  
Pressor Activity ◽  
Renal Hypertensive Rat ◽  
Renal Hypertensive Rats

The role played by circulating pressor substances in the renal hypertensive rat was studied by means of an isovolemic cross-circulation technique which is capable of detecting pressor activity in the blood of rats made hypertensive by continuous infusions of renin or synthetic angiotensin. When rats are made hypertensive by release of a completely occluded renal pedicle, this pressure elevation is transferred to an assay rat cross-circulated from the test animal several minutes after the release of the pedicle clamps. It follows that this form of renal hypertension is humorally mediated. On the contrary, when rats with renal hypertension of over 1 week's duration are cross-circulated no rise in blood pressure results in the assay rat, indicating that the maintenance of the elevated blood pressure in renal hypertension in the rat is not dependent on a circulating pressor material.

Neurogenic Activity–Angiotensin II Interaction during the Development and Maintenance of Renal Hypertension in the Rat

1979 ◽  
Vol 57 (1) ◽  
pp. 25-29 ◽  
Author(s):  
G. Bellini ◽  
R. Fiorentini ◽  
M. Fernandes ◽  
G. Onesti ◽  
H. Hessan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Vessel ◽  
Severe Hypertension ◽  
Left Kidney ◽  
Renal Hypertension ◽  
Chronic Phase ◽  
Central Effect ◽  
Delayed Response ◽  
Hypertensive Rats

1. Pentolinium tartrate (a ganglionic blocker) was injected in conscious rats during the early and late phases of two-kidney renal hypertension produced by aortic ligation. 2. In the early phase (5 days after aortic ligation), ganglionic blockade resulted in a decrease in blood pressure equal to that obtained in normotensive rats. Later, at days 12 and 40, for equally severe hypertension, ganglion blockade resulted in a greater decrease in blood pressure. 3. A 30 min infusion of [Sar1, Ala8]angiotensin II during the pentolinium-induced nadir in blood pressure resulted in a further decrease in blood pressure at day 5. Later, at days 12 and 40, this effect was smaller. 4. A 300 min infusion of [Sar1, Ala8]angiotensin II normalized the blood pressure in hypertensive rats at day 40. This delayed response may be secondary to a central effect of the antagonist, reducing neurogenic tone or peripheral antagonism of locally generated angiotensin II in the blood vessel walls. 5. At day 40, removal of the small left kidney resulted in a greater decrease in blood pressure. This suggests the presence of a renal factor other than renin in the chronic phase of this hypertension.

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.

Renin content and excretory function of the kidney in rats with experimental hypertension

1962 ◽  
Vol 202 (4) ◽  
pp. 795-799 ◽  
Author(s):  
H. Brunner ◽  
P. A. Desaulles ◽  
D. Regoli ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Hypertension ◽  
Experimental Hypertension ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Excretory Function ◽  
Contralateral Kidney ◽  
Ligation Of The Ureter ◽  
Renin Content

To determine relationship between kidney renin content and excretory function, rats with renal hypertension induced by unilateral clamping of the renal artery were given an oral load of 3 ml of 0.9% saline/100 g body wt. Excretion of the saline load was accelerated in rats with renal hypertension as well as in animals with hypertension due to overdosage with cortexone and salt, provided that the loading experiment was made 3–4 weeks after hypertension was established, but not when animals had been hypertensive for 11–14 weeks. Renin concentration was markedly reduced in the unclamped kidney and also in the kidney of the rats overdosed with cortexone and salt. Excreting capacity of the clamped kidney was compared with that of the unclamped kidney, after removal or after functional elimination of the contralateral kidney, by ligation of the ureter, 3, 24, and 48 hr after the operation. In all experiments excretion of saline load by the unclamped kidney was more rapid than by the clamped kidney, but the highest values were reached in the presence of a functional clamped kidney. Only in rats with elevated blood pressure was the load more rapidly excreted than in normal rats, but hypertension alone cannot be the only factor responsible, the excretion not being accelerated in unilaterally nephrectomized hypertensive rats. Although these hint at a connection between the renin concentration and renal function the nature of this relationship remains uncertain.

Effect of baroreceptor denervation on stimulation of drinking by angiotensin II in conscious dogs

1991 ◽  
Vol 260 (3) ◽  
pp. E333-E337 ◽  
Author(s):  
C. K. Klingbeil ◽  
V. L. Brooks ◽  
E. W. Quillen ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Plasma Angiotensin ◽  
High Doses ◽  
Stimulation Of

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.

Effects of third-generation β-blockers, atenolol or amlodipine on blood pressure variability and target organ damage in spontaneously hypertensive rats

2020 ◽  
Vol 38 (3) ◽  
pp. 536-545 ◽  
Author(s):  
Julieta S. Del Mauro ◽  
Paula D. Prince ◽  
Miguel A. Allo ◽  
Yanina Santander Plantamura ◽  
Marcela A. Morettón ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Variability ◽  
Spontaneously Hypertensive Rats ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Target Organ ◽  
Third Generation ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Β Blockers
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