Potassium currents in frog ventricular muscle: evidence from voltage clamp currents and extracellular K accumulation.

Abstract

The single sucrose voltage clamp technique was used to control the membrane potential of frog ventricular muscle strips and to measure the membrane current. The extracellular K accumulation ([K]o) was estimated from the after-potential observed after the release of the voltage clamp. Comparing the time course of the membrane current to the development of the after-potential at different membrane potentials, all slow current changes are related to changes in the K current across the membrane. Based on measurements of membrane current and the after-potential, the total membrane current was separated into 2 fractions the K current which gives rise to K accumulation and the residual membrane current which is unrelated to K accumulation. The current-voltage relation for the residual membrane current is linear or inwardly rectifying. Residual current is zero at the resting potential and increases to about 1 .mu.A/cm2 at -20 mV. The measured membrane currents and after-potentials indicate qualitative differences between the K currents which dominate below and above -20 mV. More negative to -20 mV the after-potential develops rapidly while at potentials positive to -20 mV the after-potential develops slowly. The current dominating below -20 mV is inwardly-rectifying. The current-voltage relation has a maximum (about 2 .mu.A/cm2) and a region with marked negative slope conductance. The outward current in the region of negative slope conductance is increased with increasing [K]o. A model for the inwardly rectifying K current is described. The model reproduces the shape of the measured current-voltage relations and their modification by alterations in the extracellular K concentration. The model is compatible with the observation that all slow current changes below -20 mV are directly related to K accumulation. The K current which dominates at potentials positive to -20 mV is activated by a potential and time dependent process which is unrelated to extracellular K accumulation. Q10 for the magnitude of the inwardly rectifying K current is about 1.35 while the Q10 for the rate of increase of the time dependent K current is about 3-4. Cs blocks the inwardly rectifying K current but has little effect on the time dependent K current. The changes in the action potential duration caused by increasing the extracellular K concentration or addition of Cs to the perfusate can be explained by the effect of K and Cs on the inwardly rectifying K current.