scholarly journals Estradiol replacement attenuates stress‐induced pressor response by regulating renin‐angiotensin system in ovariectomized rats

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Yu Nagatomo ◽  
Shoko Tazumi ◽  
Risa Itoh ◽  
Misa Yoshimoto ◽  
Akira Takamata ◽  
...  
2016 ◽  
Vol 311 (5) ◽  
pp. R898-R905 ◽  
Author(s):  
Shoko Tazumi ◽  
Naoko Yokota ◽  
Mizuho Kawakami ◽  
Sayo Omoto ◽  
Akira Takamata ◽  
...  

The purpose of this study was to determine whether chronic estrogen replacement in ovariectomized rats inhibits the pressor response to psychological stress by attenuating the activation of the renin-angiotensin system. Female Wistar rats aged 9 wk were ovariectomized. After 4 wk, the rats were randomly assigned to be implanted subcutaneously with pellets containing either 17β-estradiol (E2) or placebo (Pla). After 4 wk of treatment, the rats underwent cage-switch stress and, in a separate experiment, a subset received an infusion of angiotensin II. The cage-switch stress rapidly elevated blood pressure (BP) and heart rate (HR) as measured by radiotelemetry in both groups. However, the BP and HR responses to the stress were significantly attenuated in the E2 group compared with the Pla group. An angiotensin II type 1 receptor blocker, losartan, given in drinking water, abolished the difference in the pressor response to stress between the two groups. Moreover, the stress-induced elevation in plasma renin activity and angiotensin II concentration was significant in the Pla group, but not in the E2 group. In addition, the expression of renin mRNA in the kidney was lower in the E2 group relative to the Pla group. Finally, we found that intravenous angiotensin II infusion increased BP and decreased HR to a similar degree in both groups. These results suggest that the inhibitory effects of estrogen on psychological stress-induced activation of the renin-angiotensin system could be at least partially responsible for the suppression of the pressor responses to psychological stress seen in estrogen-replaced ovariectomized rats.


2002 ◽  
Vol 16 (1) ◽  
pp. 15-21
Author(s):  
Tomohisa Ishikawa ◽  
Hiromasa Nejishima ◽  
Takuya Imamura ◽  
Koichi Nakayama

1984 ◽  
Vol 247 (1) ◽  
pp. R15-R23 ◽  
Author(s):  
M. D. Cipolle ◽  
J. E. Zehr

Studies were conducted in freshwater turtles Pseudemys scripta to define some characteristics of the renin-angiotensin system in this reptile. Dialyzed acid-treated kidney extract (1 g tissue per ml water) produced a prolonged pressor response in unanesthetized turtles, which was eliminated by boiling the extract or by pretreating the turtle with [Sar1, Ile8]angiotensin II. A rat pressor assay was employed because turtle angiotensin (ANG) was bound poorly by the anti-[Asp1, Ile5, His9]ANG I used in our radioimmunoassay. Kidney extract incubated with homologous plasma (pH 5.5 and 25 degrees C) produced a time-dependent pressor response in rats. The pressor activity of the product was eliminated by dialysis or by pretreating the rats with [Sar1, Ile8]ANG II. The pressor response in anesthetized turtles to ANG I was significantly reduced by captopril, whereas the ANG II response remained unchanged, thus demonstrating the presence of ANG-converting enzyme activity in these animals. We determined the velocity of turtle ANG formation at various dilutions of enzyme (kidney extract) or substrate (plasma). Turtle kidney extract incubated with homologous plasma displayed typical Michaelis-Menten kinetics. Finally we conducted experiments to determine whether a portion of turtle plasma renin exists in an inactive form. Trypsinization caused a slight increase in plasma renin activity (PRA), whereas acidification to pH 3.3 yielded a fourfold increase in PRA.


1986 ◽  
Vol 251 (2) ◽  
pp. R258-R263
Author(s):  
J. C. Lee ◽  
D. M. Denbow ◽  
M. D. Ashen ◽  
A. D. Roudabush

The purpose of this investigation was to examine the possible involvement of the central renin-angiotensin system in the pressor response to the intracerebroventricular (icv) injection of hypertonic NaCl in conscious turkeys. The icv injection was accomplished via a stereotaxically implanted stainless steel guide cannula in the lateral cerebral ventricle. The arterial blood pressure (AP) of the turkey was measured by means of a PE catheter in the left brachial artery. The icv administration of hypertonic NaCl caused a dose-dependent increase of AP. The mean AP increases due to 10-microliter icv injections of 0.9, 3.6, and 7.2% NaCl were 1.4 +/- 1.4, 18.1 +/- 3.0, and 31.2 +/- 3.2 (SE) mmHg, respectively. These changes were statistically significant (P less than 0.001). The icv administration of captopril, [Sar1, Ile8]angiotensin II, or pentobarbital sodium markedly reduced the pressor response to the icv injection of hypertonic 7.2% NaCl. Blockade of central adrenergic receptors with phentolamine and propranolol was without effect. These results support the contention that the central renin-angiotensin system may directly contribute to pressor responses induced by central hypertonic NaCl stimulation.


1987 ◽  
Vol 65 (8) ◽  
pp. 1739-1751 ◽  
Author(s):  
Campbell D. Spence ◽  
John P. Coghlan ◽  
Derek A. Denton ◽  
Eric H. Mills ◽  
Mark A. Nelson ◽  
...  

The roles of the autonomic nervous system, renin–angiotensin system, and arginine vasopressin (AVP) during the onset of ACTH-induced hypertension were investigated in conscious sheep. Autonomic ganglion blockade or combined adrenergic and cholinergic receptor blockade demonstrated that an intact sympathetic nervous system was not essential for the development or maintenance of the hypertension. Autonomic blockade augmented the pressor response to ACTH, indicating that baroreceptor-mediated reflexes normally operate to suppress the degree of hypertension produced by ACTH. Evidence was obtained suggesting that the renin–angiotensin system and AVP may partially contribute to the maintenance of ACTH hypertension in the presence of autonomic blockade. However, the precise mechanism by which ACTH raises arterial pressure remains to be elucidated.


Hypertension ◽  
2008 ◽  
Vol 51 (4) ◽  
pp. 1170-1176 ◽  
Author(s):  
Julio C. Sartori-Valinotti ◽  
Radu Iliescu ◽  
Licy L. Yanes ◽  
Wanda Dorsett-Martin ◽  
Jane F. Reckelhoff

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