scholarly journals Significance of the Vascular Concentration of Angiotensin II–Receptor Blockers on the Mechanism of Lowering Blood Pressure in Spontaneously Hypertensive Rats

2013 ◽  
Vol 123 (4) ◽  
pp. 371-379 ◽  
Author(s):  
Shinji Takai ◽  
Denan Jin ◽  
Hiroshi Sakonjo ◽  
Takayuki Takubo ◽  
Toyofumi Nakanishi
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Angiotensin Ii Receptor Blockers ◽  
Angiotensin Ii Receptor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Receptor Blockers

The Intrinsic Brain Iso-Renin-Angiotensin System in the Rat: Its Possible Role in Central Mechanisms of Blood Pressure Regulation

1974 ◽  
Vol 48 (s2) ◽  
pp. 265s-268s ◽  
Author(s):  
D. Ganten ◽  
J. S. Hutchinson ◽  
P. Schelling
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Angiotensin Ii Receptor ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin

1. Angiotensin is produced by the intrinsic iso-renin-angiotensin system. 2. Angiotensin is secreted into the cerebrospinal fluid of nephrectomized rats. 3. Angiotensin in cerebrospinal fluid elevates systemic blood pressure. 4. Rats with hereditary diabetes insipidus are virtually non-responsive to intraventricular angiotensin. 5. Angiotensin II is elevated in the cerebrospinal fluid of spontaneously hypertensive rats. 6. An intraventricular perfusion of the angiotensin II receptor-blocking agent P 113 decreases blood pressure in spontaneously hypertensive rats.

scholarly journals Administration of Telmisartan Reduced Systolic Blood Pressure and Oxidative Stress Probably Through the Activation of PI3K/Akt/eNOS Pathway and NO Release in Spontaneously Hypertensive Rats

2013 ◽  
pp. 351-359 ◽  
Author(s):  
L. XU ◽  
Y. LIU
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Angiotensin Ii Receptor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
No Release ◽  
And Oxidative Stress

We investigated the effects of telmisartan, the blocker of angiotensin II receptor 1, on the regulation of systolic blood pressure (SBP) and oxidative stress through endothelial nitric oxide (NO) release in spontaneously hypertensive rats (SHRs). SHRs randomly received placebo, oral feeding of telmisartan (5 mg/kg or 10 mg/kg) every day and Wistar-Kyoto rats (WKYs) served as normotensive control. The SBP of rat was measured before and weekly thereafter. After a total of 8-week treatment, rats were killed for experimental measurements. Parameters that subject to measurements in isolated aorta endothelial cells include: NO concentration, protein expression levels of angiotensin II receptor 1, nitrotyrosine, 8-isoprostane, SOD, PI3K, Akt, AMPK and eNOS. In addition, L-NMMA, a general inhibitor of nitric oxide synthase, was also applied to test the inhibition of NO concentration. We found that SBPs were significantly lower in telmisartan therapy group than in placebo treated hypertensive rats and WKYs (p<0.05). The NO concentration was significantly higher in telmisartan-treated group with increased activity of the PI3K/Akt pathway and activated eNOS signaling. Blockade of Akt activity reversed such effects. Activation of AMPK also contributed to the phosphorylation of eNOS. L-NMMA treatment reduced less NO concentration in SHR rats than the telmisartan co-treated groups. Oxidative stress in SHRs was also attenuated by telmisartan administration, shown by reduced formation of nitrotyrosine, 8-isoprostane, and recovered SOD protein level. Telmisartan enhanced NO release by activating the PI3K/Akt system, AMPK phosphorylation and eNOS expression, which attenuated the blood pressure and oxidative stress in SHRs.

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