Immediate and Delayed Antihypertensive Effects of Angiotensin-Converting Enzyme Inhibition with Captopril

Since its introduction as an experimental antihypertensive agent, captopril (Capoten, SQ 14225) has been shown to lower blood pressure effectively in a considerable proportion of patients with essential and renovascular hypertension (1–5). The drug was designed as a specific, potent competitive inhibitor of angiotensin-converting enzyme (6) and, following oral administration to human subjects, it can block almost completely the effects of in-fused angiotensin I (7). Long-term administration of captopril to hypertensive patients results in a sustained reduction in aldosterone secretion, concomitant potassium retention and, in most cases, natriuresis (8)—effects that can be ascribed to a drug-induced reduction in circulating angiotensin II. Despite these findings, there has been considerable controversy regarding the extent to which its antihypertensive effect is mediated by blockade of the renin-angiotensin system.