Two mechanisms for positive inotropism of low-K Ringer solution in bullfrog atrium

Abstract

IT has long been known that a reduction of K concentration in external fluid immediately potentiates the twitch contraction of frog heart¹. Microelectrode studies^2,3 have revealed a hyperpolarisation of the membrane and a prolongation of the action potential, which was thought to be a cause of the potentiation of contraction. But, when the muscle is soaked in K-depleted fluid the membrane Na/K ATPase and the activity of the Na pump are inhibited⁴ and Na ions progressively accumulate within the cell⁵. In myocardium, the accumulation or rise of [Na]_i produces a secondary increase of [Ca]_i due to Na–Ca exchange diffusion and the consequent positive inotropic effect^6,7. Thus, Ehara⁸ has demonstrated the presence of a delayed potentiating effect of low-K Ringer solution possibly due to Na-pump inhibition in the frog ventricle as well as its immediate inotropic effect. We have tried to clarify further the nature of these inotropic actions. We show here that, in the frog atrium, augmentation of Ca-inward current (Ica) and increase of Ica-independent tonic tension, related to Na–Ca exchange, are responsible for the immediate and delayed inotropic effects under voltage clamp, respectively.