UNIDIRECTIONAL SODIUM AND POTASSIUM FLUX IN MYOGENIC L6 CELLS - MECHANISMS AND VOLUME-DEPENDENT REGULATION

To clarify the relative participation of particular ion transport systems in net univalent cation fluxes under basal conditions and altered volume of skeletal muscle-derived cells, the effect of inhibitors of the Na+-K+ pump (ouabain), univalent ion cotransporters [bumetanide, furosemide, and (dihydroindenyl)oxy alkanoic acid], and Na+/H+ exchanger (ethylisopropylamiloride) on Rb-86 and Na-22 flues has been studied in L6 myoblasts incubated in isosmotic (320 mosmol/kg) and anisosmotic media. Under the isosmotic condition, the relative contribution of ouabain-inhibited and ouabain-insensitive bumetanide-inhibited component of Rb-86 influx was similar to 15-20 and 60%, respectively. Na-22 influx was inhibited by bumetanide and ethylisopropylamiloride by 25 and 15%, respectively. Under isosmotic conditions, an increase of L6 cell volume was observed after addition of extracellular acetylcholine, extracellular Kf-induced depolarization, or lowering of the pH of the incubation medium. High extracellular glutathione (150 mu M) did not affect the cell volume of the muscle-derived cells bathed in isosmotic medium. Results of this study suggest that the bumetanide-inhibited component of K+ influx plays a key role in the adjustment of transmembrane K+ gradient in L6 myoblasts. The Na+/H+ exchanger appears to be important in regulatory volume increase.