Biochemical Studies on the Regulation of Myocardial Contractility

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Abstract
NEW information regarding the chemical basis for adjustments in cardiac performance has recently come to light. Short-term augmentation of contractility may be mediated by cyclic AMP through a mechanism that involves membrane phosphorylation. In addition, studies of biochemical changes that occur in cardiac hypertrophy indicate that contractile proteins are rapidly replaced in response to work overload. It has also been suggested that an abnormal myosin species underlies the defective performance of hypertrophied and failing hearts; no structural abnormality in myosin or other contractile proteins has been identified, however. Before the evidence of multiple biochemical defects in these hearts is discussed, . . .