The angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor (AR) blockers are widely used for the treatment of patients with hypertension or heart failure and patients who have had a myocardial infarction. Currently, at least 10 ACE inhibitors and 7 AR blockers are marketed in the United States.

1. Mechanism of toxicity

   1. ACE inhibitors reduce vasoconstriction and aldosterone activity by blocking the enzyme that converts angiotensin I to angiotensin II. AR blockers directly inhibit the action of angiotensin II.

   2. All the ACE inhibitors except captopril and lisinopril are prodrugs that must be metabolized to their active moieties (eg, enalapril is converted to enalaprilat) following oral administration.

   3. Angioedema and cough associated with ACE inhibitors are thought to be mediated by bradykinin, which normally is broken down by angiotensin-converting enzyme. However, it has also been rarely reported with AR blockers, which do not alter bradykinin elimination.

   4. Pharmacokinetics (see also Table II–61

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