Potassium movement during hyperpolarization of cardiac muscle.
When a bundle of cardiac muscle cells is hyperpolarized, membrane current declines with time. Voltage clamp experiments on sheep and cat ventricular bundles showed that the magnitude of inward current depended on the external K+ concentration. Following prolonged hyperpolarization, membrane current near the resting potential was generally outward. The half-time of decay of this outward current was approximately 2.5 sec at -60mV. The potential measured in the absence of externally supplied current was generally more negative than it would have been without conditioning hyperpolarization. The half-time of recovery of the current response following hyperpolarization was also approximately 2.5 sec at -60 mV, a factor of approximately 3.7 slower than the preceding decline of inward current. The rate of recovery has only a slight temperature dependence (Q10 approximately equal to 1.2). The experimental results are consistent with the idea that during hyperpolarization K+ is depleted from approximately 3% of the total muscle volume, and that the replenishment of K+ occurs primarily by K+ diffusion from a much larger fraction of the extracellular space.
D000200:Action Potentials; D000818:Animals; D001693:Biological Transport, Active; D002415:Cats; D006352:Heart Ventricles / Q000378:metabolism; D008564:Membrane Potentials; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism* / Q000502:physiology; D012756:Sheep
D011188:Potassium