Lisinopril plateau concentrations in patients with renal failure were inversely related to renal function, requiring 30-70 ng/ml for 50% inhibition of plasma ACE activity.
Lisinopril concentration is inversely related to renal function, and radioinhibitor binding studies are useful for establishing pharmacokinetic and pharmacodynamic profiles of ACE inhibitors.
Angiotensin converting enzyme (ACE) and the ACE inhibitor lisinopril were measured in patients with renal impairment, by both radioinhibitor 125I MK351A binding studies, and by radioimmunoassay. Plasma concentration of lisinopril estimated by radioinhibitor binding displacement correlated closely with that measured by radioimmunoassay. Plateau lisinopril concentration in 8 patients with varying degrees of renal failure treated with 5 mg lisinopril per day for 1 week, was inversely related to renal function. Plasma lisinopril concentrations of 30-70 ng/ml were required for 50% inhibition of plasma ACE activity in vivo. Acute studies in the rat showed inhibition of ACE in different tissues had different time courses. These observations suggest that 125I MK351A binding studies in tissues will be useful in establishing the pharmacokinetic and pharmacodynamic profiles of newer ACE inhibitors, and may help delineate the contribution of ACE in different tissues to cardiovascular homeostasis.
Johnston et al. (Thu,) conducted a other in Renal impairment (n=8). Lisinopril was evaluated on Plasma concentration of lisinopril and ACE inhibition. Lisinopril plateau concentrations in patients with renal failure were inversely related to renal function, requiring 30-70 ng/ml for 50% inhibition of plasma ACE activity.