Indexed on: 01 Dec '80Published on: 01 Dec '80Published in: Journal of Muscle Research and Cell Motility
Metabolic inhibition of frog heart by cyanide (3 × 10−3m) induced a drop in tension before any significant alteration occurred in the action potential or the slow inward current. The decline in electrical activity appeared later. After 20 min in cyanide solution at a time when both tension andIslow were reduced, the addition of adrenaline (5 × 10−7m) greatly increased the slow inward current whereas tension only exhibited a partial and slow recovery. In both types of experiment the absence of correlation between the amount of inward Ca2+ current and the tension suggested the existence of a regulatory mechanism other than this current. It was not possible to correlate the fall in tension (which was parallel to the drop in creatine phosphate) with the reduction in ATP. ATP only decreased during application of both cyanide (CN−) and iodoacetic acid (IAA). Quick-stretch and quick-release experiments, conducted during the tension which developed in the presence of CN− and IAA, showed that the mechanical activity did not result from Ca2+-activated tension but from rigor tension, implying a marked deficiency in local ATP. A shortage of the energy available for myofibrillar ATPase activity might be one explanation for the drop in peak tension during metabolic inhibition and the rise in resting tension observed after more severe inhibition might be a shortage of the energy-rich phosphates available for myofibrillar ATPase activity.