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Dissociation of actomyosin ATPase activity from myocardial function in physiologic cardiac overload
96 DISSOCIATION OF ACTOMYOSIN ATPASE ACTIVITY FROM MYOCARDIAL FUNCTION IN PHYSIOLOGIC CARDIAC OVERLOAD. J. Scheuer, T. F. Schaible, and A. Malhotra. Departments of Physiology and Medicine, Albert Einstein Col. of Med.-Montefiore Hosp. and Med. Ctr., Bronx, New York, U.S.A. In order to study the relation of increased actomyosin ATPase activity and cardiac function in physiologic overload, hearts of rats conditioned by swimming (SW) or running (R) were compared with hearts of sedentary controls. The hearts were studied in an isolated perfused working rat heart apparatus under similar heart rate, preload and afterload conditions and were analyzed for actomyosin ATPase activity SW 150 min/day for 8 weeks caused an increase in stroke volume of VW. 16 to 17% (p
THE TRIGGER MECHANISM INITIATING CARDIAC HYPERTROPHY IN SYSTOLICHYPERSchreiber, Sidney S. Department of Nuclear Medicine,Veterans TENSION. Administration Hospital, New York & Department of Medicine, New York University School of Medicine, New York, New York. Systolic hypertension in vitro and in vivo is followed by a hypertrophy response associated with increased protein synthesis. A sequence of events has been established in the in vitro preparation which shows a rapid increase in adenylcyclase activity, increased polyamine levels, augmented RNA polymerase activity initially of the Mn++ high ionic strength stimulation followed by Mg++ stimulated activity, increased synthesis of proteins by polysomes obtained from stressed ventricles and incubated in cell free systems, and increased synthesis of myosin as early as 3-4 hours after the onset of the systolic hypertension. Nuclei obtained from afterloaded ventricles will demonstrate Mn++ stimulated (mRNA type) RNA polymerase activity as early as 20 minutes after onset of stress and then show increased Mg++ stimulated activity after The translation of pressure stress to this 1 hour (ribosomal type). activity is not known, but nuclei obtained from normal ventricles and suspended in cytosol will show increased Mn++ polymerase activity after subjected to increased hydrostatic pressure produced outside the cell. This increase is abolished by an inhibitor of mRNA synthesis, a-amanitin. Thus, the trigger mechanism may be suggested as that working directly through the application of pressure on the cardiac nuclei.
THE TRIGGER MECHANISM INITIATING CARDIAC HYPERTROPHY IN SYSTOLICHYPERSchreiber, Sidney S. Department of Nuclear Medicine,Veterans TENSION. Administration Hospital, New York & Department of Medicine, New York University School of Medicine, New York, New York. Systolic hypertension in vitro and in vivo is followed by a hypertrophy response associated with increased protein synthesis. A sequence of events has been established in the in vitro preparation which shows a rapid increase in adenylcyclase activity, increased polyamine levels, augmented RNA polymerase activity initially of the Mn++ high ionic strength stimulation followed by Mg++ stimulated activity, increased synthesis of proteins by polysomes obtained from stressed ventricles and incubated in cell free systems, and increased synthesis of myosin as early as 3-4 hours after the onset of the systolic hypertension. Nuclei obtained from afterloaded ventricles will demonstrate Mn++ stimulated (mRNA type) RNA polymerase activity as early as 20 minutes after onset of stress and then show increased Mg++ stimulated activity after The translation of pressure stress to this 1 hour (ribosomal type). activity is not known, but nuclei obtained from normal ventricles and suspended in cytosol will show increased Mn++ polymerase activity after subjected to increased hydrostatic pressure produced outside the cell. This increase is abolished by an inhibitor of mRNA synthesis, a-amanitin. Thus, the trigger mechanism may be suggested as that working directly through the application of pressure on the cardiac nuclei.