Excitation-contraction coupling in frog ventricle. Possible Ca2+ transport mechanisms.

In frog ventricular muscle generation of tension was found to be under direct and continuous control of membrane potential. No phasic component of tension was found at any membrane potential. Developed tension depended only on the duration and amplitude of depolarization and was independent of previous contractile history. Developed tension, in part, depended on Ca2+ influx through a slowly inactivating component of Isi. Using long voltage clamp steps to achieve steady-state tension, no decline or reversal of developed tension was found at ECa. Increasing the [Ca]o shifted the tension-voltage relation to more negative potentials and increased the net outward current at potentials positive to -10 mV. The increase in tension seemed to be related to the increase in outward membrane current and K+ efflux, as estimated from post clamp K+ accumulations. Increasing [K]o, either by clamp-induced K+-accumulation or by increasing the [K] of the bathing solution, decreased the developed tension. These results suggest that in frog ventricular muscle Ca2+ for activation of tension is transported primarily from the extracellular space. There was no trigger-release of internal stores or recirculation of sequestered Ca2+. Activator Ca2+ was transported in part by a slowly inactivating Isi channel and a coupled transport mechanism. The exact mechanism by which Ca2+ transport and K+ efflux were related could not be identified.