The contribution of potassium accumulation to outward currents in frog atrium.

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Abstract
Voltage-clamp experiments on frog atrial muscle were designed to distinguish effects due to K accumulation in extracellular spaces from those due to activation of K conductance mechanisms in the membrane. The set of instantaneous current-voltage relations obtained at various external K concentrations following depolarization to about -10 mV for several seconds was different from that obtained before the depolarization. The process of increasing the extracellular K concentration cannot account for all the time-dependent changes in outward current during depolarization. Although the instantaneous current-voltage relations obtained at different values of external K concentration before prolonged depolarization show the crossover phenomenon, those obtained at the end of the depolarization did not show this feature. The current-voltage relations for the channels conducting the time-dependent K current do not show cross-over. A model involving K activation and K accumulation was constructed. This model successfully reproduces the appearance of a very slow component in outward current decay tails which, when subtracted by semi-exponential curve-stripping, leaves a component with the real time constant of conductance change. The model does not reproduce the appearance of a fast decaying component without adding a 2nd conductance mechanism, or assuming non-exponential decay of a single conductance mechanism. Apparently current [i]x,fast is not a perturbation of ix,slow or of iK1 by the process of K accumulation. The relative magnitude of ix,fast is not greatly changed by substantially increasing the external K concentration to reduce the proportionate effect of K accumulation on the K concentration.