Elevated extracellular potassium and caesium exert a negative inotropic effect on frog atrial trabeculae, likely secondary to reduced intracellular sodium activity affecting the Na-Ca exchange.
No immediate clinical implications for inotropy; leaves open Na-Ca exchange mediation in mammalian myocardium.
The exposure of frog atrial trabeculae to Ringer solution containing an elevated K+ concentration, produces a depolarization of the membrane and a reduction of both the duration of the action potential and the strength of the heart beat. In voltage-clamped preparations, the effect of perfusion with K+-rich Ringer solution is threefold. First, a sustained inward current develops at the holding potential (-80 mV). Secondly, the contractions evoked by depolarizing clamp pulses are reduced: this effect which is greater upon the tonic phase of the contraction than the early phasic tension, is also seen to follow the addition of Cs+ ions to the bathing fluid; at equal concentrations K+ ions are the more effective. Thirdly, when measured with an ion-sensitive micro-electrode in ventricular trabeculae, the intracellular Na+ ion activity (aiNa) declines with a time course similar to the development of the negative inotropic effect. This suggests that the actions of raised [K+]o or [Cs+]o upon tension may be secondary to an effect on the movement of Na+ ions across the cell membrane, which by reducing aiNa may affect tension by way of the Na-Ca exchange.
No takes yet. Share an insight, caveat, or question.
Chapman et al. (1987) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: