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• W1995798888 abstract "We have measured the EDTA and Ca2+ activated ATPase activity of myosin from hearts of normal dogs, dogs in gross heart failure and dogs with cardiac hypertrophy without failure. Heart failure was caused by systolic and/or diastolic hemodynamic loads. Under one or more assay conditions, depressed ATPase activity was consistently found for myosin from failing hearts. In contrast to myosin from hearts with diastolic loads, myosin from failing hearts with pulmonic stenosis in the presence of Ca2+ and 0.1 m KCl showed normal mean ATPase activity with several preparations having elevated activity. Elevated ATPase activities were obtained for myosin from the non-failing, but hypertrophied hearts of dogs with aortic stenosis. The data suggest that the interaction of ionic strength and pH with the ATPase active site of suggest that the interaction of ionic strength and pH with the ATPase active site of myosin from failing hearts is altered, thus modifying the ATPase activity in the presence of Ca2+ or EDTA. The altered interaction may be modified by the presence of hypertrophy, resulting in normal or increased activity in the presence of Ca2+ and decreased activity in the presence of EDTA." @default.
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• W1995798888 date "1975-11-01" @default.
• W1995798888 modified "2023-09-27" @default.
• W1995798888 title "The ATPase activity of cardiac myosin from failing and hypertrophied hearts" @default.
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• W1995798888 doi "https://doi.org/10.1016/0022-2828(75)90133-9" @default.
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