## Abstract

A selective survey of the literature reveals at least three major anion-dependent cation transport systems, defined as Na<latex>$^+$</latex> + Cl<latex>$^-$</latex>, K<latex>$^+$</latex> + Cl<latex>$^-$</latex> and Na<latex>$^+$</latex> + K<latex>$^+$</latex> + Cl<latex>$^-$</latex> respectively. In human red cells, kinetic data on the fraction of K<latex>$^+$</latex> and Na<latex>$^+$</latex> influx inhibitable by bumetanide are presented to indicate an Na<latex>$^+$</latex>:K<latex>$^+$</latex> stoichiometry of 1:2. For LK sheep red cells the large Cl<latex>$^-$</latex>-dependent K<latex>$^+$</latex> leak induced by swelling is shown to share many characteristics with that induced by N-ethyl maleimide (NEM) treatment. NEM has complex effects, both inhibiting and then activating Cl<latex>$^-$</latex>-dependent K<latex>$^+$</latex> fluxes dependent on NEM concentration. The alloantibody anti-L can prevent the action of NEM. In human red cells NEM induces a large Cl<latex>$^-$</latex>-dependent specific K<latex>$^+$</latex> flux, which shows saturation kinetics. Its anion preference is Cl<latex>$^-$</latex> > Br<latex>$^-$</latex> > SCN<latex>$^-$</latex> > I<latex>$^-$</latex> > NO<latex>$^-_3$</latex> > MeSO<latex>$^-_4$</latex>. This transport pathway is not inhibited by oligomycin or SITS, although phloretin and high concentrations of furosemide and bumetanide (over 0.3 mM) do inhibit. Quinine (0.5 mM) is also an inhibitor. It is concluded that at least two distinct Cl<latex>$^-$</latex>-dependent transport pathways for K<latex>$^+$</latex> are inducible in mammalian red cells, although the evidence for their separation is not absolute.