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Chronic oral administration of beta-adrenoceptor agonist clenbuterol affects myosin heavy chain (MHC) expression in adult mouse heart

S. N. Patiyal, S. Sharma

. 2007 ; 56 (3) : 275-283.

Jazyk angličtina Země Česko

Perzistentní odkaz   https://www.medvik.cz/link/bmc07502615

The aim of this study was to analyze the effects of chronic administration of the ß-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 ß-isoform of MHC in the clenbuterol-treated group. The ?: ß 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 ß-agonist-treated group. These results suggest that chronic clenbuterol treatment is capable to induced the transformation of MHC isoforms increasing the slow ß-MHC isoform, which may contribute to the altered contractile mechanics of clenbuterol-treated hearts.

Bibliografie atd.

Lit.: 33

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$a The aim of this study was to analyze the effects of chronic administration of the ß-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 ß-isoform of MHC in the clenbuterol-treated group. The ?: ß 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 ß-agonist-treated group. These results suggest that chronic clenbuterol treatment is capable to induced the transformation of MHC isoforms increasing the slow ß-MHC isoform, which may contribute to the altered contractile mechanics of clenbuterol-treated hearts.
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