PROTEIN-SYNTHESIS DURING REGRESSION OF LEFT-VENTRICULAR HYPERTROPHY WITH LISINOPRIL IN ABDOMINAL AORTIC CONSTRICTION MODEL OF HYPERTENSION

The use of lisinopril was assessed in inducing regression of establish ed left ventricular hypertrophy. Left ventricular hypertrophy was achi eved by aortic constriction in the rat, Lisinopril was administered in drinking water (5 mg/kg body weight/day) to aortic constricted rats s tarting from Day 30 for a period of further 30 days. At the end of 60 days the rates of protein synthesis were measured using the flooding d ose technique, Lisinopril reduced the mixed protein contents of the re gressed left ventricle from 223 +/- 7 mg to 175 +/- 10 mg/left ventric le in the aortic constricted rats; P < 0.01, all data are means +/- SE M, n = 5-8, The regression of left ventricular mass occurred along wit h simultaneous decrease in the rate of protein synthesis (i.e., 6.56 /- 0.33 in aortic constricted rats versus 4.40 +/- 0.44%/ day, in lisi nopril treated left ventricles, P < 0.05). However, the expanded cardi ocyte fiber thickness remained unchanged despite lisinopril treatment (i.e., 20.4 +/- 0.7 in aortic constricted rats versus 19.5 +/- 0.6 mu m in regressed left ventricles, P > 0.05). The results indicate that r egression of pressure overloaded hypertrophy with lisinopril primarily occurs by a decrease in protein synthesis in the connective tissue co mponents of the left ventricle, although cytoskeletal components may b e unaffected. (C) 1996 Academic Press, Inc.