Lisinopril: a nonsulfhydryl angiotensin-converting enzyme inhibitor.

The chemistry, pharmacology, pharmacokinetics, clinical use, adverse effects, and dosage of lisinopril are reviewed. Lisinopril, a new nonsulfhydryl angiotensin-converting-enzyme (ACE) inhibitor, is absorbed in its active form. Like the other ACE inhibitors, it lowers peripheral vascular resistance, with a resultant decrease in blood pressure. Approximately 29% of lisinopril is absorbed after oral administration. No measurable metabolism occurs, and excretion is primarily renal. Accumulation of lisinopril occurs in patients with renal dysfunction; however, dosage adjustment is necessary only when the creatinine clearance is less than 30 mL/min. Lisinopril has been shown to be an effective antihypertensive agent at doses of 10 to 80 mg given once daily in patients with essential and secondary hypertension caused by renal artery stenosis. The effectiveness of lisinopril is comparable to that with diuretics, beta blockers, and calcium-channel antagonists. In patients who are unresponsive to maximal doses of lisinopril alone, addition of another antihypertensive agent may be beneficial. Limited information suggests that lisinopril may be comparable to captopril for the treatment of congestive heart failure. Adverse effects associated with lisinopril are relatively minor and are comparable to those associated with enalapril. Hematological abnormalities have not been reported with lisinopril. Class-related adverse effects include cough, azotemia, angioedema, hypotension, and hyperkalemia. Lisinopril appears to be comparable to other ACE inhibitors for the treatment of hypertension and may be as effective as its predecessors for the treatment of congestive heart failure. Further study is needed to better define a therapeutic niche for lisinopril.