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Cardiovascular Research 1981 15(11):637-642; doi:10.1093/cvr/15.11.637
© 1981 by European Society of Cardiology
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Copyright © 1981, European Society of Cardiology

Circulatory and renin responses in man to unilateral reduction of the renal perfusion pressure

MAURIZIO D GUAZZI*, CESARE FIORENTINI, MARIA T OLIVARI, ANTONIO BARTORELLI, FABIO MAGRINI and CARLA BIANCARDI

From the Istituto Ricerche Cardiovascular "Giorgio Sisini", Centro Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Cattedra di Cardiologia, University of Milan, Milan, Italy

* Correspondence and reprint request should be addressed to: Maurizio D Guazzi, MD, lstituto Ricerche Cardiovascolari. Via Bonfadini 214, 20138 Milano, Italy.

This study is concerned with the mechanisms of human renovascular hypertension. Unilateral partial occlusion of a renal artery was accomplished using a balloon-tipped catheter for occlusive angiography in seven normotensive and 17 primary hypertensive subjects. The renin and circulatory responses were studied during a 60 min reduction of the renal perfusion pressure (RPP) by 50% of control. This stimulus was considered to be safe and strong enough to produce a three to four-fold rise in plasma renin activity. It was observed that: a) systemic (arterial) renin was significantly raised at 5 min, reached a peak at 15 min and continued to be significantly higher than the baseline until the occlusion was removed; b) venous renin and venous arterial difference on the occluded side became elevated after the stimulus and remained so for the duration of the occlusion: c) renin release from the contralateral kidney became partially inhibited; d) in no case did systemic arterial pressure, heart rate or cardiac output change during the studies: e) renin and circulatory patterns were similar in normotensive and hypertensive subjects.

It is concluded that in humans unilateral RPP reduction duplicates the renin pattern of the Goldblatt kidney, but does not duplicate the circulatory response. This evidence applies to a 1 h renal artery occlusion and does not exclude the possibility that renin may have a role in a rise in blood pressure following renal artery stenosis of longer duration.


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