scholarly journals Genistein alleviates renin-angiotensin system mediated vascular and kidney alterations in renovascular hypertensive rats

2022 ◽  
Vol 146 ◽  
pp. 112601
Author(s):  
Anuson Poasakate ◽  
Putcharawipa Maneesai ◽  
Prapassorn Potue ◽  
Sarawoot Bunbupha ◽  
Terdthai Tong-Un ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Renin Angiotensin

Role of Prostaglandins on the Renin-Angiotensin System in Normotensive and Hypertensive Rats

1996 ◽  
Vol 26 (2) ◽  
pp. 553
Author(s):  
Pyung-Jin Yoon ◽  
Mann Jung ◽  
Jong-Seung Kim ◽  
Jae-Yeoul Jun ◽  
Cheol-Ho Yeum
Keyword(s):  
Renin Angiotensin System ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Renin Angiotensin

Renin-angiotensin system in stroke-prone spontaneously hypertensive rats

1979 ◽  
Vol 236 (3) ◽  
pp. H409-H416 ◽  
Author(s):  
M. Shibota ◽  
A. Nagaoka ◽  
A. Shino ◽  
T. Fujita
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Malignant Hypertension ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin

The development of malignant hypertension was studied in stroke-prone spontaneously hypertensive rats (SHR) kept on 1% NaCl as drinking water. Along with salt-loading, blood pressure gradually increased and reached a severe hypertensive level (greater than 230 mmHg), which was followed by increases in urinary protein (greater than 100 (mg/250 g body wt)/day) and plasma renin concentration (PRC, from 18.9 +/- 0.1 to 51.2 +/- 19.4 (ng/ml)/h, mean +/- SD). At this stage, renal small arteries and arterioles showed severe sclerosis and fibrinoid necrosis. Stroke was observed within a week after the onset of these renal abnormalities. The dose of exogenous angiotensin II (AII) producing 30 mmHg rise in blood pressure increased with the elevation of PRC, from 22 +/- 12 to 75 +/- 36 ng/kg, which was comparable to that in rats on water. The fall of blood pressure due to an AII inhibitor, [1-sarcosine, 8-alanine]AII (10(microgram/kg)/min for 40 min) became more prominent with the increase in PRC in salt-loaded rats, but was not detected in rats on water. These findings suggest that the activation of renin-angiotensin system participates in malignant hypertension of salt-loaded stroke-prone SHR rats that show stroke signs, proteinuria, hyperreninemia, and renovascular changes.

The role of the renin-angiotensin system and oxidative stress in spontaneously hypertensive rat mesenteric collateral growth impairment

2007 ◽  
Vol 292 (5) ◽  
pp. H2523-H2531 ◽  
Author(s):  
Steven J. Miller ◽  
Laura E. Norton ◽  
Michael P. Murphy ◽  
Michael C. Dalsing ◽  
Joseph L. Unthank
Keyword(s):  
Renin Angiotensin System ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin ◽  
Growth Impairment ◽  
Collateral Growth ◽  
Collateral Artery

Recent clinical and animal studies have shown that collateral artery growth is impaired in the presence of vascular risk factors, including hypertension. Available evidence suggests that angiotensin-converting enzyme inhibitors (ACEI) promote collateral growth in both hypertensive humans and animals; however, the specific mechanisms are not established. This study evaluated the hypothesis that collateral growth impairment in hypertension is mediated by excess superoxide produced by NAD(P)H oxidase in response to stimulation of the ANG II type 1 receptor. After ileal artery ligation, mesenteric collateral growth did not occur in untreated, young, spontaneously hypertensive rats. Significant luminal expansion occurred in collaterals of spontaneously hypertensive rats treated with the superoxide dismutase mimetic tempol, the NAD(P)H oxidase inhibitor apocynin, and the ACEI captopril, but not ANG II type 1 (losartan) or type 2 (PD-123319) receptor blockers. The ACEI enalapril produced equivalent reduction of arterial pressure as captopril but did not promote luminal expansion. This suggests the effects of captopril on collateral growth might result from its antioxidant properties. RT-PCR demonstrated that ANG II type 1 receptor and angiotensinogen expression was reduced in collaterals of untreated rats. This local suppression of the renin angiotensin system provides a potential explanation for the lack of effect of enalapril and losartan on collateral growth. The results demonstrate the capability of antioxidant therapies, including captopril, to reverse impaired collateral artery growth and the novel finding that components of the local renin angiotensin system are naturally suppressed in collaterals.

scholarly journals Difference in the vascular renin-angiotensin system in two types of renovascular hypertensive rats

1995 ◽  
Vol 67 ◽  
pp. 264 ◽  
Author(s):  
Tomoko Tokioka ◽  
Masayuki Shibasaki ◽  
Akira Fujimori ◽  
Osama Inagaki ◽  
Wataru Uchida ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Renin Angiotensin

Differential effect of tetradecythioacetic acid on the renin-angiotensin system and blood pressure in SHR and 2-kidney, 1-clip hypertension

2007 ◽  
Vol 293 (3) ◽  
pp. F839-F845 ◽  
Author(s):  
Liliana Monica Bivol ◽  
Rolf Kristian Berge ◽  
Bjarne Magnus Iversen
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Reduction ◽  
Kidney Tissue ◽  
Renin Angiotensin System ◽  
Minor Effect ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Blood Pressure Lowering Effect ◽  
Angiotensin System ◽  
Renin Angiotensin

The tetradecythioacetic acid (TTA) is a modified fatty acid known to exhibit pleiotropic effects. First, we compared the effect of TTA on the blood pressure in spontaneously hypertensive rats (SHR) with two-kidney, one-clip (2K1C)-hypertensive rats. Second, we examined mechanisms involved in the blood pressure reduction. TTA had minor effect on systolic blood pressure (SBP) in young SHR up to 8 wk of age. In 2K1C we confirmed the blood pressure-lowering effect of TTA (SBP: 173 ± 4 before vs. 138 ± 3 mmHg after TTA, P < 0.001). No effect on SBP was seen in Wistar-Kyoto rat (WKY) controls. Plasma renin activity (PRA) was low in SHR and WKY controls and TTA did not change it. PRA decreased from 22.9 ± 1.3 to 16.2 ± 2.2 ng·ml−1·h−1 ( P = 0.02) in 2K1C. Plasma ANG II concentration declined from 101 ± 3 to 81 ± 5 fmol/l after TTA treatment ( P = 0.005). In the clipped kidney, tissue ANG I concentration decreased from 933 ± 68 to 518 ± 60 fmol/g tissue ( P = 0.001), and ANG II decreased from 527 ± 38 to 149 ± 21 fmol/g tissue ( P < 0.001) after TTA treatment. In the nonclipped kidney, TTA did not change ANG I and moderately reduced ANG II levels. The renal blood flow response to injection of ANG II into the nonclipped kidney was blunted compared with controls and normalized with TTA treatment (10 ± 2 before vs. 20 ± 2%, P < 0.001). The results indicate that TTA downregulates the renin-angiotensin system in high renin animals but has no effect in low renin models.

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