Potassium (using 86Rb+ as a tracer), amino acid and taurine fluxes were measured in horse red blood cells (RBCs). No volume-sensitive component of alanine and glycine transport was observed, and although volume-sensitive taurine fluxes were observed in most animals, their absolute magnitudes were small. K+ fluxes, however, were shown to be particularly volume sensitive; they were stimulated by cell swelling and inhibited by cell shrinkage. Sizeable fluxes were present at normal cell volumes. The volume-sensitive K+ flux was Cl- dependent and was abolished by Cl- replacement with methylsulphate. The Cl(-)-dependent K+ fluxes in horse red blood cells were stimulated by lowering in external pH to 6.9 and by treatment with the sulphydryl-reacting agent, N-ethylmaleimide. They were inhibited by the potent K(+)-Cl- co-transport inhibitor, DIOA, ([(dihydroindenyl)oxy]alkanoic acid) but were insensitive to the Na(+)-K(+)-Cl- co-transport inhibitors, frusemide and bumetanide. A Cl- channel inhibitor, 5-nitro-2-(phenylpropyl-amino)-benzoate (NPPB), produced partial inhibition. These results suggest that regulatory volume decrease in horse red blood cells is achieved predominantly by volume-sensitive K+ efflux mediated via a K(+)-Cl- co-transport system with similar properties to those observed in the red blood cells of other species. The significance of these findings and their rheological consequences are discussed.

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