Abstract
The application of methods with a fine time resolution to the study of metabolic events following administration of E to the perfused rat heart has shown that the increased force of contraction occurs prior to an elevation in the level of phosphorylase a. It is concluded, therefore, that neither energy produced from glycogenolysis nor an intermediate of glycogen breakdown is involved in the initiation of the inotropic response. Cyclic 3',5'-AMP does, however, appear to be involved, but in a manner which remains to be elucidated. In cardiac muscle, when glucose is present, E enhances both the rate of glycogen breakdown and the rate of glycogen synthesis.
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