The heart's physiological performance, unlike that of skeletal muscle, is regulated primarily by variations in the contractile force developed by the individual myocardial fibers. In an attempt to identify the basis for the characteristic properties of myocardial contraction, the individual cardiac contractile proteins and their behavior in contractile models in vitro have been examined. The low shortening velocity of heart muscle appears to reflect the weak ATPase activity of cardiac myosin, but this enzymatic activity probably does not determine active state intensity. Quantification of the effects of Ca++ upon cardiac actomyosin supports the view that myocardial contractility can be modified by changes in the amount of calcium released during excitation-contraction coupling. Exchange of intracellular K+ with Na+ derived from the extracellular space also could enhance myocardial contractility directly, as highly purified cardiac actomyosin is stimulated when K+ is replaced by an equimolar amount of Na+. On the other hand, cardiac glycosides and catecholamines, agents which greatly increase the contractility of the intact heart, were found to be without significant actions upon highly purified reconstituted cardiac actomyosin.
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Article| July 01 1967
Regulation of Cardiac Muscle Contractility
Arnold M. Katz
From the Department of Physiology, College of Physicians and Surgeons, Columbia University, New York.
Dr. Katz's present address is the Department of Medicine, The University of Chicago
Online Issn: 1540-7748
Print Issn: 0022-1295
Copyright © 1967 by The Rockefeller University Press
J Gen Physiol (1967) 50 (6): 185–196.
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Arnold M. Katz; Regulation of Cardiac Muscle Contractility . J Gen Physiol 1 July 1967; 50 (6): 185–196. doi: https://doi.org/10.1085/jgp.50.6.185
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