Potassium (using Rb-86+ as a tracer), amino acid and taurine fluxes we
re measured in horse red blood cells (RBCs). No volume-sensitive compo
nent of alanine and glycine transport was observed, and although volum
e-sensitive taurine fluxes were observed in most animals, their absolu
te magnitudes were small. K+ fluxes, however, were shown to be particu
larly volume sensitive; they were stimulated by cell swelling and inhi
bited by cell shrinkage. Sizeable fluxes were present at normal cell v
olumes. The volume-sensitive K+ flux was Cl- dependent and was abolish
ed by Cl- replacement with methylsulphate. The Cl--dependent K+ fluxes
in horse red blood cells were stimulated by lowering in external pH t
o 6.9 and by treatment with the sulphydryl-reacting agent, N-ethylmale
imide. They were inhibited by the potent K+-Cl- co-transport inhibitor
, DIOA, ([(dihydroindenyl)oxy]alkanoic acid) but were insensitive to t
he Na+-K+-Cl- co-transport inhibitors, frusemide and bumetanide. A Cl-
channel inhibitor, 5-nitro-2-(phenylpropyl-amino)-benzoate (NPPB), pr
oduced partial inhibition. These results suggest that regulatory volum
e decrease in horse red blood cells is achieved predominantly by volum
e-sensitive K+ efflux mediated via a K+-Cl- co-transport system with s
imilar properties to those observed in the red blood cells of other sp
ecies. The significance of these findings and their rheological conseq
uences are discussed.