Heart muscle. Intracellular potassium and inward-going rectification.
The cellular K content of frog ventricular strips is monitored using 42K. Cellular K loss evoked by cardiac glycosides or a low extracellular K concentration is accompanied by a more than proportional decrease in the conductance of the resting membrane and the rate of rapid repolarization of the action potential. Voltage clamp experiments relate these changes to a decrease in the magnitude of an inward-rectifying K current. Current-voltage relations measured before and after changing the extracellular K concentration cross each other. This violation of the independence principle has previously suggested that extracellular K ions are required to open the rectifier channel (Cleemann and Morad. 1979. J. Physiol. 286: 113). Decreasing the cellular K content decreases the outward membrane current at all membrane potentials by an amount that is consistent with the independence principle. This suggests that the gating process is not sensitive to intracellular K ions. These findings are consistent with a previously published model for inward-going rectification.
D000818:Animals; D006321:Heart / Q000502:physiology*; D008564:Membrane Potentials; D011188:Potassium / Q000378:metabolism*; D011898:Ranidae; D013816:Thermodynamics
D011188:Potassium