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Pharmacology: Pharmacodynamics: Enalapril is an angiotensin converting enzyme inhibitors, acts primarily through suppression of the renin-angiotensin-aldosterone system.
Following oral administration, enalapril is rapidly absorbed and then hydrolysed to enalaprilat, which a highly specific, long-acting, non-sulfhydryl angiotensin-converting enzyme inhibitors.
It prevents the conversion of angiotensin I to angiotensin II by inhibiting angiotensin converting enzyme (ACE) and also inhibit local angiotensin II at vascular and renal sites and attenuate the release of catecholamine from adrenal nerve endings.
Inhibiting ACE results in decrease plasma angiotensin II and increased plasma renin activity (PRA). This leads to decrease aldosterone secretion, resulting in small increase in serum potassium, and sodium and fluid loss.
Enalaprilat produce a reduction of peripheral arterial resistance in hypertensive patients, and either no change or an increase in cardiac output. Renal blood flow increases, but glomerular filtration rate is usually unchanged. Peak blood pressure reduction is achieved by 4 to 6 hours. To achieve maximum effects, several weeks of therapy may be required.
Pharmacokinetics: Enalapril maleate is rapidly absorbed from gastro-intestinal tract, approximately 60% of a dose is absorbed and peak serum concentrations occur within about one hour. Enalapril absorption is not influenced by the presence of food.
Enalapril is metabolised in the liver by hydrolysis to enalaprilat, the active metabolite. Excretion of enalapriat and enalapril is primarily renal.
Approximately 94% of the dose is recovered in the urine and feces as enalaprilat or enalapril. The principle components in urine are enalaprilat, accounting for about 40% of the dose, and intact Enalapril. The elimination half-life is approximately 11 hours, and is increased in patients with renal failure.
