Electromechanical responsiveness of hyperthyroid cardiac muscle to beta-adrenergic stimulation.

The effect of isoproterenol (5 x 10(-10)-10(-6) M) on simultaneous measurements of the transmembrane action potential (TAP) and isometric twitch were made in thin right ventricular papillary muscles isolated from hyperthyroid (H) and euthyroid (E) rats. In response to low concentrations of isoproterenol (less than 5 x 10(-9) M) both TAP depolarization above -40 mV and twitch tension were significantly enhanced in H (30 and 50% above base line, respectively) but were not changed in E. The maximum catecholamine-induced change in twitch tension and TAP was not different in H versus E. However, over the entire dose-response curve to isoproterenol, the relaxant effects of the catecholamine, i.e., shortening of the times from stimulus to peak tension (TPT) and from stimulus to half-relaxation of tension (RT 1/2) that accompanied twitch potentiation and TAP changes in E did not occur in H. In contrast to the absence of a relaxant effect on these twitch duration parameters in H, the rate of tension decay of the terminal part of the twitch was enhanced in H to an extent equal to that in E. The results suggest that 1) in response to low levels of beta-adrenergic stimulation, enhanced TAP depolarization above -40 mV, which occurs in H but not in E, mediates the twitch potentiation that occurs in H but not in E; 2) the cellular mechanisms that mediate twitch potentiation and action potential changes in response to beta-adrenergic stimulation are independent of those that control the relaxant effect to shorten TPT; and 3) factors through which catecholamines enhance the rate of tension decay in the terminal phase of the contraction cycle are independent of those that reduce TPT and RT 1/2; thus beta-adrenergic stimulation appears to have a "dual" relaxant effect on the myocardium.