Mechanism of activation of contraction in frog ventricular muscle.

Publisher Website
Google Scholar
Abstract
The force of contraction and transmembrane potential was 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 Ca concentration) had no detectable effect on subsequent contractions. An increase in extracellular Ca 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 expected if a Ca 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 Ca concentration. Force development occurring after displacement of transmembrane potential to levels beyond the equilibrium potential for Ca was rapidly sensitive to alterations in extracellular composition, including addition of 10 mM Mn2+, an increase in Ca concentration and a decrease in Na concentration. The source of Ca for activation of contraction in frog ventricular muscle apparently 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. Such transsarcolemmal Ca movement is brought about by driving forces which add to those of electrodiffusion.