Depression of myosin B by catecholamine analogs: mechanism and in vivo significance

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Abstract
Catecholamine analogs (beta receptor blocking agents) DCI [dichloroisoproterenol], DCE [dichloroepinephrine], DCA [dehydroxy corticosterone acetate], pronethalol, propranolol, MJ-1999 [4-(2-isopropylamino-1-hydroxyethyl] methane sulfonanilide], methoxamine, and phenylephrine delay superprecipitation of myosin B. Analogs also inhibit ATPase activity and syneresis of myosin B, and of cardiac myofibrils, but are without effect on mitochondria or mitochondrial extracts. Propranolol was most potent, DCA lease. As in the intact animal [dog], the depressant effects of analogs could be fully reversed by high concentrations of either catecholamines or Ca. When tested on Ca-buffered myosin B, analogs shifted the concentration-effect curve for Ca to the right, but did not alter the maximum effect attained at high Ca concentrations. Analogs alter the affinity of myosin B for Ca; depression of contraction produced by analogs in living muscle is due to impaired utilization of ATP. When taken together with the stimulant effect of catecholamines on syneresis of cardiac fibrils, the effects of analogs support the view that the beta adrenergic inotropic receptor in cardiac muscle is a constituent of myosin B.