AJP - Heart and Circulatory Physiology, Vol 251, Issue 5 897-H902, Copyright © 1986 by American Physiological Society
Renal vasodilatation after inhibition of renin or converting enzyme in marmoset
D. Neisius, J. M. Wood and K. G. Hofbauer
The relative importance of angiotensin II for the renal vasodilatory
response after converting-enzyme inhibition was evaluated by a comparison
of the effects of converting-enzyme and renin inhibition on renal vascular
resistance. Renal, mesenteric, and hindquarter blood flows were measured
with chronically implanted ultrasonic-pulsed Doppler flow probes in
conscious, mildly volume-depleted marmosets after administration of a
converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin
inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal
antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16
+/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27
+/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in
blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5,
respectively) and selective increases in renal blood flow (36 +/- 12%, n =
6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular
resistance was of similar magnitude for all of the inhibitors (enalaprilat
-28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results
indicate that the renal vasodilatation induced after converting-enzyme or
renin inhibition is mainly due to decreased formation of angiotensin II.
