Hypertension, Vol 23, 44-51, Copyright © 1994 by American Heart Association
ND Fisher, D Allan, I Kifor, CL Gaboury, GH Williams, TJ Moore and NK Hollenberg
We compared the renal vascular responses to angiotensin converting enzyme
inhibition and renin inhibition to assess the influence of angiotensin II
(Ang II). We examined the renal and endocrine responses to the renin
inhibitor enalkiren, to captopril, and to placebo in nine healthy and nine
hypertensive men on a 10-mmol sodium diet. Ang II was infused to assess
effects of the agents on renal and adrenal responsiveness to Ang II. Plasma
Ang II concentration was suppressed similarly with enalkiren and
captopril--an identical level of blockade was achieved. Although renal
plasma flow was stable during placebo, a substantial rise was seen with
both enalkiren (+133 +/- 26 mL/min per 1.73 m2) and captopril (+99.4 +/-
22.6). There was remarkable intrasubject concordance between the renal
plasma flow responses to renin inhibition and converting enzyme inhibition
(r = .90, P < .004). The vasodilator response to both agents correlated
inversely with the fall in renal plasma flow induced by Ang II alone (r =
-.66, P < .05). Both agents significantly enhanced the renal vascular
response to Ang II (P = .01), and, furthermore, the renal vasodilator
response to captopril predicted the potentiation of the renal plasma flow
response to Ang II after either agent (enalkiren: r = .91, P < .001;
captopril: r = .56, P < .05). Concordance of the maximal renal plasma
flow response to the two agents appeared in the hypertensive men as well.
Our results indicate that the acute renal response to captopril largely
reflects a reduction in Ang II formation.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Responses to converting enzyme and renin inhibition. Role of angiotensin II in humans
Department of Medicine, Harvard Medical School, Boston, Mass.
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