Angiotensin-Converting Enzyme Inhibitors


Joseph L. Izzo, Jr, MD, Department of Medicine, Erie County Medical Center, 462 Grider Street, Buffalo, NY 14215


J Clin Hypertens (Greenwich). 2011;13:667–675. ©2011 Wiley Periodicals, Inc.

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).