The soluble cardiac relaxing system may constitute an intracellular site of action for adrenergic mediators in heart muscle, providing a biochemical mechanism for their effect on cardiac contraction.
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Adrenergic effects on cardiac ATPase may involve the soluble relaxing system; leaves open any physiological role in intact myocardium.
The influence of adrenergic mediators on the Mg-stimulated actomyosin ATPase of glycerinated cardiac myofibrils was analyzed. The mediators increased ATPase activity in the presence of soluble cardiac relaxing substance, but were without effect in its absence. Mechanical changes in the fibrils accompanied changes in ATPase activity. Threshold concentrations were: dl-isoproterenol = 3 x 10 –8 m, l-epinephrine = 7 x 10 –8 m, and l-norepinephrine = 6 x 10 –7 m. Dichloroisoproterenol and dichloroepinephrine decreased ATPase activity in both the presence and absence of relaxing substance. The depressant effects of the dichloro analogs were not altered by epinephrine and isoproterenol, and could account for adrenergic "blockade" in vivo. Evidence of the specificity of myofibrillar enzyme, relaxing substance, and adrenergic stimulus is presented. Comparison of the properties of the cardiac inotropic adrenergic receptor with the properties of the soluble cardiac relaxing system suggests that the latter constitutes an intracellular site of action of adrenergic mediators in heart muscle.
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Stam et al. (1965) studied this question.
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