Net sodium influx under K-free conditions was independent of the intracellular sodium ion concentration, [Na]i, and was increased by ouabain. Unidirectional sodium influx was the sum of a component independent of [Na]i and a component that increased linearly with increasing [Na]i. Net influx of sodium ions in K-free solutions varied with the external sodium ion concentration, [Na]o, and a steady-state balance of the sodium ion fluxes occurred at [Na]o = 40 mM. When solutions were K-free and contained 10-4 M ouabain, net sodium influx varied linearly with [Na]o and a steady state for the intracellular sodium was observed at [Na]o = 13 mM. The steady state observed in the presence of ouabain was the result of a pump-leak balance as the external sodium ion concentration with which the muscle sodium would be in equilibrium, under these conditions, was 0.11 mM. The rate constant for total potassium loss to K-free Ringer solution was independent of [Na]i but dependent on [Na]o. Replacing external NaCl with MgCl2 brought about reductions in net potassium efflux. Ouabain was without effect on net potassium efflux in K-free Ringer solution with [Na]o = 120 mM, but increased potassium efflux in a medium with NaCl replaced by MgCl2. When muscles were enriched with sodium ions, potassium efflux into K-free, Mg++-substituted Ringer solution fell to around 0.1 pmol/cm2·s and was increased 14-fold by addition of ouabain.

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