Abstract
The aim of this study was to analyze the effects of chronic administration of the beta-adrenoceptor agonist clenbuterol (2 mg/kg body weight/day for a period of 30 days) on the major contractile protein (myosin) in the left ventricular muscle of the adult mouse heart. Separation of myosin heavy chain (MHC) isoforms on 7.5 % glycerol SDS-PAGE and subsequent quantification of the gels by laser densitometry showed a 6.5-fold increase in the beta-isoform of MHC in the clenbuterol-treated group. The alpha : beta ratio of these two isoforms in the control group was 98.16+/-0.14 %: 1.83+/-0.14 %, whereas in the treated group it was 88.05+/-1.15 % : 11.95+/-1.15 %. Actomyosin ATPase activity assay demonstrated a significant (20 %) decline in ATPase activity of the tissue in the beta-agonist-treated group. These results suggest that chronic clenbuterol treatment is capable to induced the transformation of MHC isoforms increasing the slow beta-MHC isoform, which may contribute to the altered contractile mechanics of clenbuterol-treated hearts.
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