CAUSE OF THE PROLONGED PRESSOR ACTION OF RENIN IN NEPHRECTOMIZED RATS

Elucidated by Means of Anti-Angiotensin II and of Angiotensin-Inhibitor (l-Sar-8-Ala-Angiotensin II)

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Abstract

In nephrectomized rats, both the primary and the prolonged pressor response to exogenous renin, the duration of which markedly exceeds the rate of disappearance of renin activity from plasma, is shown to be due to the continued action of renin, the blood pressure being totally or subtotally normalized by infusion of an angiotensin inhibitor. A marked, but somewhat less pronounced, decrease in the blood pressure is caused by injection of anti-angiotensin II. An accumulation of renin in the arterioles may account for these results. The height of the pressor response to renin is identical in anaesthetized and conscious normal rats, but the length is markedly shorter in anaesthetized than in conscious animals.

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