Myosin isoenzyme changes in several models of rat cardiac hypertrophy.

• DOI: 10.1161/01.res.49.2.525
• Publication Date: 2012-06-12T00:17:09Z
• Authors: J J Mercadier; A M Lompré; C Wisnewsky; J L Samuel; J Bercovici; B Swynghedauw; K Schwartz
• Keywords: Contractility; Pressure overload

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