Mechanism of activation of contraction in frog ventricular muscle.

Abstract

SUMMARY The force of contraction and transmembrane potential were recorded from extremely short segments of frog ventricle strips, in which extracellular ionic composition could be changed rapidly, and a condition in which there was a relatively uniform space clamp. Large and abrupt increases in contractile force (and, presumably, in intracellular free calcium concentration) had no detectable effect on subsequent contractions. In contrast, an increase in extracellular calcium concentration was associated with a progressive increase in contraction extending over several beats. Displacement of transmembrane potential during an action potential affected contraction in a manner opposite to that to be expected if a calcium current were to play a significant role in activation. The activation process could be saturated by sufficient displacement of transmembrane potential to high inside positive levels. The voltage displacement necessary for saturation was less the higher the extracellular calcium concentration. Force development occurring after displacement of transmembrane potential to levels beyond the equilibrium potential for calcium was rapidly sensitive to alterations in extracellular composition, including addition of 10 mti Mn 2+ , an increase in calcium concentration, and a decrease in sodium concentration. These observations provide further evidence that the source of calcium for activation of contraction in frog ventricular muscle consists exclusively, or almost exclusively, of an influx of this ion into the cell. This process contributes throughout the range of voltage dependence of activation: i.e., from threshold to saturation. The observations suggest that such transsarcolemmal calcium movement is brought about by driving forces which add to those of electrodiffusion.