Potassium efflux in heart muscle during activity: extracellular accumulation and its implications.

Publisher Website
Google Scholar
Abstract
Extracellular K+ activity and transmembrane potential were simultaneously monitored with a K+ selective micro-electrode placed in the extracellular space and a standard KCl-filled micro-electrode in the intracellular space of the frog [Rana pipiens] ventricular muscle. K+ accumulated during activity and had the approximate magnitude and time course to account for the measured membrane depolarization. The magnitude of the K+ accumulation depended on the frequency of stimulation, diameter of the muscle and temperature of the bathing solution. The time constants of accumulation and decay were dependent only on the diameter and the temperature of the strip. A Q10 [change in rate of a process when temperature is increased by 10.degree. C] of 2 was measured for the decay of accumulated K+. Double barreled K+-electrodes were used to monitor the change in K+ activity accompanying a single action potential, since the reference barrel allowed for rapid compensation of the electrical potential fluctuations encountered in the subendothelial space. K+ accumulated continuously during the plateau to a level which increased external K concentration by about 1 mM. This increase in the subendothelial space corresponds to about 1-3 .mu.A/cm2 or 10-30 pmol/cm2 .cntdot. s-1 of net K+ efflux. These values are at least an order of magnitude larger than required to discharge the membrane capacity. There is no direct relation between action potential duration and rate of development or magnitude of K+ accumulation during that action potential. Increase in the external K concentration, while shortening the action potential and depolarizing the membrane, does not lead to an increased rate of accumulation of K+. The presence of Ni2+ prolongs the action potential and decreases the rate of K+ accumulation. There appears to be a substantial and continuous efflux of K+ during the action potential, which sums during rapid beating, resulting in membrane depolarization and alteration of action potential duration. The change in action potential duration in response to rate may be caused by alteration of EK [equilibrium potential for K ions] in the local micro-environments.