Abstract
The effects of procaine on the contractility of the bullfrog''s ventricular muscle were investigated. The addition of 10-5 g/ml of procaine potentiated the twitch tension which was accompanied by an elevation as well as a prolongation of the action potential plateau. This positive inotropism of procaine was not induced by endogenous catecholamine because a .beta.-blocking agent did not influence this twitch potentiation. The twitch potentiation was increased in proportion ot the external Ca concentration, suggesting the possibility of augmentation of Ca influx during the action potential. In normal Ringer solution, procaine suppressed K contracture which was composed of 2 components: an initial phasic component and a late tonic one. K contracture after perfusion with Cafree solution was also suppressed by procaine. K contracture which had been treated previously with La was composed of only a tonic component and was potentiated by procaine in spite of perfusion with Ca-free solution. The tonic component of K contracure may be considered to occur with intracellular Ca. Procaine may increase the Ca inward current, acting on the intracellular Ca storage site and consequently accelerate the excitation-contraction coupling in frog ventricular muscle.