With the availability of orally active angiotensin converting enzyme (ACE) inhibitors, it has become possible to chronically inhibit the renin-angiotensin system. When given to hypertensive patients as monotherapy, these agents can normalize the blood pressure in about 50% of all cases like other antihypertensive drugs. If the monotherapy is not sufficient to normalize blood pressure, the addition of a sodium depletion, for instance by administering concomitantly a diuretic, can become necessary to normalize blood pressure. The antihypertensive effect of ACE inhibitors is characterized by some particularly favorable features: ACE inhibitors attenuate the fall in serum potassium and the rise in plasma uric acid induced by diuretics, they do not cause any salt retention nor orthostatic hypotension, they do not raise pulse rate when they reduce blood pressure, and they certainly do not reduce the perfusion rate of the brain, the heart or the kidneys. The same features are apparent when using these agents in patients with congestive heart failure, in whom these drugs enhance cardiac output and exercise capacity by decreasing simultaneously pre- and afterload to the heart. Untoward effects of ACE inhibitors are relatively infrequent and they can mostly be foreseen based on an understanding of the pharmacological mechanisms of these compounds. Thus, with appropriate use, untoward effects are often completely avoided. Recent clinical studies have suggested that ACE inhibitors, when compared to other antihypertensive drugs, can improve the quality of life.(ABSTRACT TRUNCATED AT 250 WORDS)