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   <subfield code="a">Captopril does not acutely modulate plasma endothelin-1 concentration in human congestive heart failure</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[O. Grenier, F. Pousset, R. Isnard, H. Kalotka, A. Carayon, G. Maistre, P. Lechat, C. Guerot, D. Thomas, M. Komajda]</subfield>
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   <subfield code="a">Summary: Congestive heart failure (CHF) is a syndrome characterized by increased levels of angiotensin II (Ang II) and endothelin-1 (ET-1). In vitro, Ang II stimulates ET-1 release. The purpose of this study was to assess the effect of a single dose of an angiotensin-converting enzyme inhibitor (ACEI) captopril versus placebo on plasma endothelin concentration in human congestive heart failure. Captopril (25 mg, given orally) was compared with placebo in a group of 20 patients with systolic dysfunction in a double-blind randomized study. Plasma irET concentration was significantly increased in CHF patients compared with normal subjects (5.59 pg/ml±0.35 vs. 3.58 pg/ml±0.99, p&lt;0.0002). Despite the decrease in systolic blood pressure and the increase in plasma renin activity, suggesting a significant blockade of the renin-angiotensin system, no difference in plasma irET-1 was observed between captopril and placebo. Our results suggest that captopril does not acutely influence irET-1 plasma concentration in human CHF. These data do not support the hypothesis that the acute vasodilator effect of a single dose of 25 mg of captopril given orally involves modulation of the increased plasma concentration of endothelin observed in CHF.</subfield>
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   <subfield code="a">endothelin</subfield>
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   <subfield code="t">Cardiovascular Drugs and Therapy</subfield>
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