Vasopressin and renin response to plasma volume loss in spontaneously hypertensive rats

1986 ◽  
Vol 250 (3) ◽  
pp. H443-H452 ◽  
Author(s):  
C. D. Sladek ◽  
M. L. Blair ◽  
Y. H. Chen ◽  
R. W. Rockhold
Keyword(s):  
Plasma Volume ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin ◽  
Old Rats ◽  
Wistar Kyoto ◽  
Renin Content

Abnormalities in the vasopressin (VP) and renin-angiotensin systems have been described in spontaneously hypertensive rats (SHR). Responsiveness of these systems to a decrease in plasma volume was examined in the SHR at 6, 8, and 18 wk of age and compared with responses in age-matched normotensive Wistar and Wistar Kyoto rats (WKY). Trunk blood was collected 3 h after administration of 2 ml/100 g body wt of 0.9% saline, 15 or 30% polyethylene glycol (PEG), and in one group of conscious 8- and 18-wk-old rats, mean arterial pressure was monitored following PEG administration. Hematocrit and serum VP increased significantly in both strains at all ages following PEG. At 6 and 8 wk of age, the VP response to the PEG injection was significantly greater in SHR compared with WKY (P less than 0.005), but at 18 wk the response was comparable in the two strains. Serum renin activity (SRA) also increased in both strains receiving PEG at 6 and 8 wk of age, but the response was suppressed in the SHR relative to the WKY (P less than 0.001). At 18 wk of age, SRA increased in WKY, but the response was totally suppressed in SHR. Renal renin content in a separate group of rats was reduced in 19-wk-old SHR compared with WKY (P less than 0.001) but was not different in 5- and 8-wk-old rats. Thus there appears to be a hyperresponsiveness in the VP system in young SHRs that is not present in the renin-angiotensin system. The divergence in the responsiveness of the renin and VP systems and the attenuation of responsiveness in the VP system in 18-wk SHRs indicate a differential effect of the hypertensive process on the VP and renin systems in the SHR.

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.

Cardiovascular hypertrophy in diabetic spontaneously hypertensive rats: optimizing blockade of the renin–angiotensin system

2003 ◽  
Vol 104 (4) ◽  
pp. 341-347 ◽  
Author(s):  
Markus LASSILA ◽  
Belinda J. DAVIS ◽  
Terri J. ALLEN ◽  
Louise M. BURRELL ◽  
Mark E. COOPER ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Calcium Channel ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
At1 Receptor ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin

The aim of the present study was to compare the antihypertrophic effects of blockade of the renin–angiotensin system (RAS), vasopeptidase inhibition and calcium channel antagonism on cardiac and vascular hypertrophy in diabetic spontaneously hypertensive rats (SHR). SHR with streptozotocin-induced diabetes were treated with one of the following therapies for 32 weeks: the angiotensin-converting enzyme (ACE) inhibitor captopril (100mg/kg); the angiotensin AT1 receptor antagonist valsartan (30mg/kg); a combination of captopril with valsartan; the vasopeptidase inhibitor mixanpril (100mg/kg); or the calcium channel antagonist amlodipine (6mg/kg). Systolic blood pressure and cardiac and mesenteric artery hypertrophy were assessed. Mean systolic blood pressure in diabetic SHR (200±5mmHg) was reduced by captopril (162±5mmHg), valsartan (173±5mmHg), mixanpril (176±2mmHg) and amlodipine (159±4mmHg), and was further reduced by the combination of captopril with valsartan (131±5mmHg). Captopril, valsartan and mixanpril reduced heart and left ventricle weights by approx. 10%. The combination of captopril and valsartan further reduced heart weight (-24%) and left ventricular weight (-29%). Amlodipine did not affect cardiac hypertrophy. Only mixanpril and the combination of captopril and valsartan significantly reduced mesenteric weight. The mesenteric wall/lumen ratio was reduced by all drugs, and to a greater extent by the combination of captopril and valsartan. We conclude that optimizing the blockade of vasoconstrictive pathways such as the RAS, particularly with the combination of ACE inhibition and AT1 receptor antagonism, is associated with antitrophic effects in the context of diabetes and hypertension. In contrast, calcium channel blockade, despite similar effects on blood pressure, confers less antitrophic effects in the diabetic heart and blood vessels.

Modulation of blood pressure and the renin-angiotensin system in transgenic and spontaneously hypertensive rats after ovariectomy

1993 ◽  
Vol 11 (5) ◽  
pp. S226???S227 ◽  
Author(s):  
J??rgen Bachmann ◽  
J??rgen Wagner ◽  
Christoph Haufe ◽  
Andrzej Wystrychowski ◽  
Antonin Ciechanowicz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin
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