Angiotensin-converting enzyme inhibitors

Abstract

KEY POINTS AND RECOMMENDATIONS: • In addition to hypertension, angiotensin-converting enzyme inhibitors are indicated for treatment of patients at high risk for coronary artery disease, after myocardial infarction, with dilated cardiomypathy, or with chronic kidney disease. • The most familiar angiotensin-converting enzyme subtype, angiotensin-converting enzyme-1 (kininase II), cleaves the vasoconstrictor octapeptide angiotensin II from its inactive decapeptide precursor, angiotensin I, while simultaneously inactivating the vasodilator bradykinin. • Biochemical pathways within and around the renin-angiotensin system are highly species-specific; there is little evidence that "angiotensin-converting enzyme bypass pathways" have major clinical implications in humans. • Dietary sodium loading can diminish or abolish the antihypertensive effect of an angiotensin-converting enzyme inhibitor, while salt restriction or concomitant diuretic therapy enhances it. • Dose-response curves with angiotensin-converting enzyme inhibitors are quite flat but their peak effects vary in different individuals. • Increased serum creatinine (decreased glomerular filtration rate) during acute or chronic angiotensin-converting enzyme inhibition identifies individuals likely to experience long-term renal protective benefits. • Angiotensin-converting enzyme inhibitors are contraindicated in pregnancy due to fetal toxicity. • Use of angiotensin-converting enzymes can be limited by idiosyncratic reactions (cough or angioedema), hyperkalemia (usually in cardiac or renal failure or with combined renin-angiotensin blockade) or hypotension (usually with severe volume-depletion or cardiac failure).