From the Departments of Medicine and Pharmacology, Vanderbilt University
Medical Center (N.J.B., D.E.V.), and the Veterans Administration Medical
Center (D.E.V.), Nashville, Tenn.
Correspondence to Nancy J. Brown, MD, 560 MRB-I, Vanderbilt University Medical Center, Nashville, TN 37232-6602. E-mail nancy.brown{at}mcmail.vanderbilt.edu
Abstract
AbstractACE inhibitors
have achieved widespread usage in the treatment of
cardiovascular and renal disease. ACE
inhibitors alter the balance between the
vasoconstrictive, salt-retentive, and hypertrophic
properties of angiotensin II (Ang II) and the vasodilatory
and natriuretic properties of bradykinin and alter the
metabolism of a number of other vasoactive substances. ACE
inhibitors differ in the chemical structure of their active
moieties, in potency, in bioavailability, in plasma half-life, in route
of elimination, in their distribution and affinity for tissue-bound
ACE, and in whether they are administered as prodrugs. Thus, the side
effects of ACE inhibitors can be divided into those that
are class specific and those that relate to specific agents. ACE
inhibitors decrease systemic vascular resistance without
increasing heart rate and promote natriuresis. They have proved
effective in the treatment of hypertension, they decrease mortality in
congestive heart failure and left ventricular dysfunction
after myocardial infarction, and they delay the progression of diabetic
nephropathy. Ongoing studies will elucidate the effect of
ACE inhibitors on cardiovascular mortality
in essential hypertension, the role of ACE inhibitors in
patients without ventricular dysfunction after myocardial
infarction, and the role of ACE inhibitors compared with
newly available angiotensin AT1 receptor
antagonists.
© 1998 American Heart Association, Inc.
Cardiovascular Drugs
Angiotensin-Converting Enzyme Inhibitors
Key Words: angiotensin blood pressure bradykinin drugs renin
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