Abstract
To determine whether catecholamines produce alterations in myocardial myosin-actin cycling kinetics, we investigated the effects of isoproterenol upon mechanical characteristics of constantly activated heart muscle thought to reflect crossbridge behavior. In isolated rabbit right ventricular papillary muscles in barium contracture at 24 degrees C, we found that 10 microM isoproterenol caused: (a) a 23% reduction of the 10 to 90% rise time of slow tension recovery in force transients induced by rapid, small amplitude stretches; and (b) a 23% increase in the frequency of sinusoidal length perturbation at which stiffness amplitude exhibited a minimum. Based upon previous mechanistic interpretations of force transients, and on an analysis developed here to relate crossbridge events to the frequency-dependence of stiffness, we argue that our observations provide evidence that isoproterenol induces an acceleration of crossbridge cycling rate. This raises the intriguing prospect that beta-adrenergic stimulation regulates contraction, not only by well-known alterations in calcium metabolism, but also by intrinsic modulation of the force-generating machinery itself.
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