Abstract
In frog [Rana catesbeiana] 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) was already attained. The initial phase apparently is independent from Na-pump inhibition. Voltage clamp study revealed that the slow inward Ca current (ICa) was enhanced transiently after K depletion concomitant with an augmentation of ICa-dependent phasic tension. ICa-independent tonic tension was not altered at this initial phase. For the enhancement of ICa, 2 mechanisms appeared to be involved: one, an enhancement of .hivin.gCa; and the other, a faster and/or longer opening of the slow channel. An enhancement of ICa, together with the well-known prolongation of action potential, was the cause of the initial positive inotropic effect of K depletion.