Abstract
Calmodulin and cAMP were demonstrated to have no stimulating effect on Ca2+ transport in the sarcoplasmic reticulum of the dog heart in experimental myocardial infarction as compared to that in the uninvolved myocardium (control). Introduction to the incubation medium of exogenous protein kinase in addition to calmodulin and cAMP provoked an approximately 35% increase in 45Ca accumulation in microsomes of the impaired myocardium as compared with the system containing no exogenous protein kinase. Under the same conditions, the control showed a 75% increase in 45Ca accumulation. A reduction in the activity of Ca2+-activated ATPase of the reticulum and translocation of calmodulin activity from the membrane fraction of cardiomyocytes to cytosol were recorded in myocardial infarction.
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