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European Heart Journal 1986 7(10):877-884;
Copyright © 1986 by the European Society of Cardiology.
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© 1986 The European Society of Cardiology

The renal response to neuroendocrine inhibition in chronic heart failure: double-blind comparison of captopril and prazosin

J. BAYLISS*,{dagger}, R. CANEPA-ANSON{dagger}, M. NORELL*, P. POOLE-WILSON{dagger} and G. SUTTON*,

*Hillingdon Hospital Uxbridge, Middlesex
{dagger}The National Heart Hospital and The Cardiothoracic London, U.K.

revised 7 March 1986; accepted 17 September 1985.

Address for Correspondence: Dr G. C. Sutton, Hillingdon Hospital, Uxbridge, Middlesex, England.

Abstract

Activation of the renin–angiotensin and sympathetic systems in chronic heart failure causes important renal vasoconstriction. In a double-blind cross-over study, treatment with captopril for one month reduced systemic and renal vascular resistance by 14% and 25%, increased renal blood flow by 12%, and increased the percentage of the cardiac output perfusion to the kidney by 13%. Treatment with prazosin for one month also reduced systemic vascular resistance by 8%, renal vascular resistance increased by 20%, and renal blood flow and the percentage of the cardiac output going to the kidney fell by 14% and 26%. During captopril treatment, plasma aldosterone concentration was reduced to normal, but during prazosin treatment there was an initial increase in aldosterone of 45%, and a sustained increase in plasma noradrenaline concentration of 26%. Body weight decreased by 1.7kg on captopril, but increased by 3.0 kg on prazosin, correlating inversely with the changes in renal blood flow. Sympathetic inhibition with prazosin causes systemic vasodilatation which diverts blood from the kidney and may result in fluid retention. Inhibition of the renin system with captopril causes preferential renal vasodilatation and can improve renal perfusion in chronic heart failure.

Key Words: Renal vasodilatation • heart failure • captopril • prazosin


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