The principal components in urine are enalaprilat, accounting for about 40 percent of the dose, and intact enalapril. Approximately 94 percent of the dose is recovered in the urine and feces as enalaprilat or enalapril. Peak serum concentrations of enalaprilat occur three to four hours after an oral dose of enalapril maleate. Following absorption, enalapril is hydrolyzed to enalaprilat, which is a more potent angiotensin-converting enzyme inhibitor than enalapril enalaprilat is poorly absorbed when administered orally. Enalapril absorption is not influenced by the presence of food in the gastrointestinal tract. Based on urinary recovery, the extent of absorption of enalapril is approximately 60 percent. Although Vasotec was antihypertensive in all races studied, black hypertensive patients (usually a low-renin hypertensive population) had a smaller average response to enalapril monotherapy than non-black patients.įollowing oral administration of Vasotec, peak serum concentrations of enalapril occur within about one hour. While the mechanism through which Vasotec lowers blood pressure is believed to be primarily suppression of the renin-angiotensin-aldosterone system, Vasotec is antihypertensive even in patients with low-renin hypertension. Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of Vasotec remains to be elucidated. Removal of angiotensin II negative feedback on renin secretion leads to increased plasma renin activity.ĪCE is identical to kininase, an enzyme that degrades bradykinin. In patients treated with Vasotec plus a thiazide diuretic, there was essentially no change in serum potassium (see PRECAUTIONS). In hypertensive patients treated with Vasotec alone for up to 48 weeks, mean increases in serum potassium of approximately 0.2 mEq/L were observed. Although the latter decrease is small, it results in small increases of serum potassium. Inhibition of ACE results in decreased plasma angiotensin II, which leads to decreased vasopressor activity and to decreased aldosterone secretion. The beneficial effects of enalapril in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin-aldosterone system. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Related/similar drugs amlodipine, lisinopril, metoprolol, losartan, furosemide, carvedilol, hydrochlorothiazide Vasotec - Clinical PharmacologyĮnalapril, after hydrolysis to enalaprilat, inhibits angiotensin-converting enzyme (ACE) in human subjects and animals.
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