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- W2000979260 abstract "Abstract The individual and combined physiological and myofibrillar protein phosphorylation effects of the negative inotropic agents, cadmium (3 × 10 −3 m m ) and lead (3 × 10 −4 m m ), and the positive inotropic agents isoproterenol (7 × 10 −7 m ) and calcium (6.5 m m ) were examined in isolated modified perfused rat heart preparations to evaluate possible causal associations between cadmium- and lead-induced changes in myofibrillar protein phosphorylations and altered inotropic responsiveness. Cadmium and lead alone depressed cardiac contractility and only the phosphorylation of the myosin light chain-2 (LC-2). These effects were attenuated in the presence of isoproterenol and elevated extracellular calcium; however, cadmium and lead inhibited both the positive inotropic activation of the heart by calcium and isoproterenol and the concomitant increase in phosphorylations of the purported cardioregulatory phospho-proteins, LC-2 and the troponin inhibitory subunit (TN-I). Positive chronotropic responses to the β-adrenergic agonist were unaffected by cadmium and lead. These results suggest that the negative inotropic effects of cadmium and lead are related to depressed phosphorylation of LC-2 and TN-I. Furthermore, the present findings suggest that cadmium and lead may alter myofibrillar protein phosphorylation mechanisms by antagonizing sarcolemmal calcium translocation processes; however, these results do not preclude the possibility of direct intracellular antagonisms of calcium-dependent processes by these heavy metal ions." @default.
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- W2000979260 date "1980-08-01" @default.
- W2000979260 modified "2023-09-23" @default.
- W2000979260 title "Influence of isoproterenol and calcium on cadmium- or lead-induced negative inotropy related to cardiac myofibrillar protein phosphorylations in perfused rat heart" @default.
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- W2000979260 doi "https://doi.org/10.1016/0041-008x(80)90214-8" @default.
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