Immediate converting-enzyme inhibition with intravenous enalapril in chronic congestive heart failure

Spencer H. Kubo, Robert J. Cody, John H. Laragh, Xavier E. Prida, Steven A. Atlas, Zhung Yuan, Jean E. Sealey

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To test the hypothesis that intravenous enalapril is a useful pharmacologic probe of the renin angiotensin system, intravenous enalapril was administered to 9 patients with severe congestive heart failure (CHF). This produced abrupt and complete blockade of converting enzyme, with peak effect occurring at 30 minutes, as reflected by increases of plasma renin activity (from 16.8 ± 6 to 86.6 ± 23 ng/ml/hour) and decreases of plasma aldosterone levels (from 46 ± 14 to 25 ± 6 ng%) (both p < 0.05). With reduction of angiotensin II-mediated vasoconstriction, systemic vascular resistance decreased markedly (from 1,974 ± 233 to 1,400 ± 136 dyne s cm-5) and cardiac index was improved (from 1.88 ± 0.9 to 2.20 ± 0.21 liters/min/m2) (both p < 0.05). The time course of angiotensin II levels suggested that the lack of a cumulative effect from additive doses of intravenous enalapril was a reflection of complete inhibition of converting enzyme. One patient did not respond to enalapril; despite comparable hemodynamic severity of CHF, the renin-angiotensin system was not activated in this patient. Thus, intravenous enalapril is capable of rapid and complete inhibition of converting enzyme for the accurate assessment of angiotensin II-mediated vasoconstriction in patients with severe CHF.

Original languageEnglish
Pages (from-to)122-126
Number of pages5
JournalAmerican Journal of Cardiology
Issue number1
StatePublished - 1 Jan 1985
Externally publishedYes


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