Why the study?
Does angiotensin II antagonism reduce arterial pressure in experimental rabbit models of renal hypertension?
Does angiotensin II antagonism reduce arterial pressure in experimental rabbit models of renal hypertension?
This study demonstrates that chronic two-kidney experimental renal hypertension in rabbits is not dependent on elevated angiotensin II levels, whereas one-kidney hypertension exhibits variable dependence.
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Animal data show limited A-II dependence in most rabbit renal hypertension models; leaves open differential renin-angiotensin roles in human renovascular disease.
Hypertension was produced in rabbits by constricting the left renal artery; in nine rabbits the opposite kidney was removed and in eight rabbits the opposite kidney was left intact. To investigate the role of angiotensin II (A-II), 1-sarcosine-8-alanine angiotensin II, a competitive antagonist of A-II, was infused at 6 mug/min per kg body wt for 30 min. In a control group of seven unilaterally nephrectomized rabbits mean arterial pressure averaged 81 mmHg and infusion of the A-II antagonist did not alter the arterial pressure. In a group of Na-depleted rabbits, arterial pressure decreased from 81 to 63 mmHg (P less than 0.01) in response to the A-II analogue. Thirty days after renal artery constriction, seven of the nine one-kidney hypertensive rabbits had normal values for plasma renin activity (PRA) and during infusion of the A-II antagonist arterial pressure was unchanged. However, two rabbits had elevated PRA and the arterial pressure decreased during infusion of the angiotension analogue. In the two-kidney hypertensive rabbits, PRA was normal and arterial pressure was unchanged by infusion of the A-II antagonist. These studies provide evidence that hypertension developed with either a high or normal A-II plasma level in the one-kidney animals; the two-kidney rabbits developed chronic hypertension in which no role for A-II could be demonstrated.
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Johnson et al. (1975) studied this question.
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