Circulation Research, Vol 49, 525-532, Copyright © 1981 by American Heart Association

ARTICLES

Myosin isoenzyme changes in several models of rat cardiac hypertrophy

JJ Mercadier, AM Lompre, C Wisnewsky, JL Samuel, J Bercovici, B Swynghedauw and K Schwartz

We studied the effect of chronic mechanical overloading on the isoenzyme composition of rat cardiac myosin in several experimental models: aortic stenosis (AS), aortic incompetence (AI), aortocaval fistula (ACF), overload of the non-infarcted area after left coronary ligation (INF), and overload of the spontaneously hypertensive rats (SHR). Samples of the left and right ventricles were isolated from these hearts, and myosins were analyzed by electrophoresis in non- dissociating conditions. The myosin isoenzymes were called V1, V2, and V3 in order of decreasing mobility, according to the nomenclature of Hoh et al. Controls of the Wistar and Wistar Kyoto (WKY) strains were almost exclusively V1, A slow age-dependent shift toward V3 was observed in the left ventricles of adult Wistar rats, which at 30 weeks of age (body weight 600 g) contained approximately 15% of this form. In all models of cardiac hypertrophy, an isoenzymic redistribution was observed with a significant increase in V3. The level of V3 was statistically correlated with the degree of hypertrophy in the AS, (n = 11, r - 0.6, P less than 0.05), the AI (n = 14, 4 = 0.88, P less than 0.001), and the AS + AI(n = 14, 4 = 0.69, P less than 0.01) but not in the ACF (n = 16, r = 0.46). The isoenzymic changes could account for the decreases in both myosin ATPase activity and cardiac contractility described previously in our laboratory and by others. They also demonstrate that changes in myosin isoenzymes represent a general response of the rat heart, to chronic mechanical overloading.

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