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Journal of Applied Physiology, Vol 78, Issue 1 272-281, Copyright © 1995 by American Physiological Society
ARTICLES |
C. K. Sen, O. Hanninen and S. N. Orlov
Department of Physiology, University of Kuopio, Finland.
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 N+/H+ exchanger (ethylisopropylamiloride) on 86Rb and 22Na fluxes 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 86Rb influx was approximately 15-20 and 60%, respectively. 22Na 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 K(+)-induced depolarization, or lowering of the pH of the incubation medium. High extracellular glutathione (150 microM) 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.
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