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Differences between angiotensin-converting enzyme inhibitors and receptor blockers

Timothy W Smith, MD, PhD
James P Morgan, MD, PhD
Section Editor
George L Bakris, MD
Deputy Editor
John P Forman, MD, MSc


Angiotensin-converting enzyme (ACE) inhibitors are widely used in the treatment of hypertension. They have also been effective in a number of other disorders, prolonging survival in patients with heart failure, coronary heart disease, and acute myocardial infarction, and slowing the rate of progression in chronic renal failure, particularly diabetic nephropathy. One limiting side effect in a minority of patients is cough, a side effect that does not appear to occur with increased frequency with the angiotensin receptor blockers (ARBs), which are as effective as the ACE inhibitors in the treatment of hypertension [1]. (See "Renin-angiotensin system inhibition in the treatment of hypertension".)

The evidence that there are clinically important differences between these two classes of drugs will be reviewed here. The major side effects of these drugs are discussed separately. (See "Major side effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers".)


Angiotensin II is an oligopeptide of eight amino acids, formed from its precursor, angiotensinogen by a series of two enzymatic cleavages. Angiotensinogen is released into the circulation by the liver. Renin, produced by the kidney, in response to glomerular hypoperfusion, catalyzes cleavage of angiotensinogen to angiotensin I, an inactive decapeptide. Angiotensin I is in turn cleaved by angiotensin-converting enzyme (ACE) to produce angiotensin II. Angiotensin II binds to its specific receptors and exert its effects in the brain, kidney, adrenal, vascular wall, and the heart.

There are two well-described subtypes of angiotensin II receptors, designated AT1 and AT2, both of which have a high affinity for angiotensin II [2,3]:

The AT1 subtype mediates the vasoconstrictor effect of angiotensin II and is generally thought to mediate angiotensin II-induced growth in the left ventricle and the arterial wall [4].


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Literature review current through: Sep 2016. | This topic last updated: Mar 1, 2016.
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