Soluble cardiac relaxing factor likely controls contractile strength through a mechanism beyond simple calcium chelation.
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Does not support calcium chelation by cardiac relaxing factor; leaves open distinct mechanisms regulating myocardial contractility.
The action of soluble cardiac relaxing substance (RS) on the Mg-stimulated actomyosin ATPase of cardiac myofibrils was studied as a function of Ca concentration. Though 2.5 x 10 –6 m soluble Ca inhibits skeletal relaxing substance, between 8 x 10 –6 and 1 x 10 –3 m ionized Ca were without effect on cardiac relaxing substance. It is concluded that the mechanism by which cardiac RS influences ATP hydrolysis involves more than simple chelation of ionized Ca. If these experiments describe the in vivo behavior of cardiac RS it seems likely that the particulate relaxing factor functions in excitation-contraction coupling and the soluble relaxing factor solely as a control of contractile strength.
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Honig et al. (1962) studied this question.
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