The angiotensin-converting enzyme inhibitor (ACEI), enalapril maleate, is a nonsulfydryl group—containing compound. Accordingly, it is said to be less associated with side effects such as taste disturbance, rashes, proteinuria, and interstitial nephritis; these side effects having been observed with captopril, and attributed to its sulfydryl group. Enalapril is a pro-drug. Because the active compound, enalaprilic acid, is poorly absorbed, the drug is given as an absorbable ester, which is then hydrolyzed to the active compound. This results in a more gradual onset of antihypertensive effect than may be seen with captopril. However, enalapril is a more potent ACEI than captopril, and its pharmacologic half-life is prolonged, permitting once daily dosage.
See also p 2358.
The consequences of ACEI therapy are complex, multidimensional, and imperfectly understood.1 The inhibition of the enzyme that converts the inactive decapeptide angiotensin-I into the potent pressor agent angiotensin-II has systemic and intrarenal consequences. Systemically, decreased