MYOSIN ISOZYMES DURING THE REGRESSION OF CARDIAC HYPERTROPHY

Abstract

An early, transient decrease in cardiac function occurs during regression (R) of pressure overload (P) left ventricular hypertrophy (LVH) in rats. This may occur because of a mismatch between the LVP and the form of myosin isozymes. We compared myosin isozymes using native gel electrophoresis in control (C), hypertrophy (H), and regression (R), rat hearts. LVH was induced by partial occulsion (O) of the ascending aorta. O was released in a group of the H rats allowing R to occur, C, H, and R rats were studied 1-4 wks. after release of O. C rats had 85% V1 myosin in all groups. H had 45% V1, 33% V2, 22% V3 at R-1 wk. (3 wk of H) and 48, 32 and 20%, respectively at R-4 wk (6 wk of H). In the 1 wk R rats the relative amounts of V1, V2 and V3 remained unchanged (43, 30, 27%, respectively). However, after 4 wk of R, rather than the isozymes forms returning to that of controls, the relative amount of V3, actually increased, 36% V1, 32% V2, 32% V3. At no time was there a shift back to V1 despite complete relief of P which occurs immediately upon release of O. Regression of LVH is nearly complete by 1 wk LV/body weight C-2,67, H-4.06, R-2.80. In this study, we found an increase in the relative amount of V3 in the absence of pressure overload in young rats after the regression of LVH. This unusual mismatch between myosin isozyme and physiologic status could be explained by an undetermined anomaly in the cardiac function during regression. A change affecting the responsive expression of V3 could also occur.