Humoral and Hemodynamic Effects

We studied the renin and the circulatory responses to unilateral reduction of the renal perfusion pressure (RPP) in seven normotensive subjects and 17 patients with primary hypertension who required diagnostic renal angiography. A balloon-tipped catheter was used for occlusive arteriography; the same catheter was also used to reduce, through appropriate inflation of the balloon, the RPP by 50% of control. In preliminary observations, this stimulus was shown to be safe and strong enough to activate renin release maximally. The reduction in RPP (either right or left) was maintained for 60 minutes. Plasma renin activity was determined after 1 hour of recumbency (baseline), at various periods during occlusion of the vessel, and after release. Cardiac output was measured at the same periods, and systemic arterial pressure and heart rate were monitored continuously. As regards the renin response, we observed that (1) systemic (arterial) renin was already significantly augmented at 5 minutes, reached a peak at 15 minutes and then tended to decrease, although the mean values continued to be markedly higher than the baseline values; (2) soon after the stimulus, venous renin and venous arterial difference of the occluded kidney became definitely elevated and remained elevated for the duration of the occlusion; (3) on the contralateral side, the venous arterial difference decreased progressively until 30 minutes after occlusion, when it was almost abolished, indicating that renin release from the nonoccluded kidney was suppressed; and (4) the response was quantitatively and qualitatively similar in normotensive and hypertensive subjects. Despite this humoral reaction, in no case did systemic arterial pressure, heart rate and cardiac output change throughout the studies. We conclude that in man, either normotensive or hypertensive, unilateral RPP reduction duplicates the renin pattern of the Goldblatt kidney, but does not duplicate the circulatory response. This evidence applies to 1-hour renal artery occlusion and does not exclude the possibility that renin may have a role in the blood pressure elevation after long-standing renal arterial stenosis.