In frog atrium, K depletion exerts initial, and late positive inotropic effects. The initial effect on the membrane potential, current and tension components was studied using a double gap method under voltage clamped and unclamped conditions. In both cases, the presence of the initial effect was demonstrated. The effect was clearer in preparations in which a positive inotropic effect to toxic doses of ouabain (10^-6 M) had already been attained. This suggests that the initial phase is independent from Na-pump inhibition. Voltage clamp study revealed that the slow inward calcium current (I_Ca) was enhanced transiently after K depletion concomitant with an augmentation of I_Ca-dependent phasic tension.I_Ca-independent tonic tension was not altered at this initial phase. For the enhancement of I_Ca, two mechanisms appeared to be involved, one an enhancement of g_Ca and the other a faster and/or longer opening of the slow channel.
These results indicated that an enhancement of I_Ca together with the wellknown prolongation of action potential were the cause of the initial positive inotropic effect of K depletion.