Action of di- and tri-valent cations on calcium-activated K+-efflux in rat erythrocytes.

Isolated rat erythrocytes were labelled with [86Rb] as a tracer for intracellular K+. It was demonstrated that rat erythrocytes possess a Ca2+-mediated K+-efflux mechanism similar to that reported for human erythrocytes. This model was used to investigate the interactions of di- and tri-valent cations on potassium [86Rb] permeability in intact cells. Low concentrations of Ag2+ and Hg2+ haemolysed erythrocytes and Pb2+ produced a selective increase in [86Rb] efflux which became self-inhibitory at concentrations above 100 microM. The effects of Pb2+ were potentiated by A23187. Ni2+, Cu2+, Co2+, Zn2+, Fe2+, Mn2+, Y2+ and Ba2+ did not initiate [86Rb] efflux, even in the presence of 0.5 microM A23187 and at concentrations as high as 1 mM. All of these cations, except Ba2+, were potent inhibitors of [86Rb] efflux evoked by 50 microM Ca2+ + 0.5 microM A23187. The lanthanides Tb3+, Gd3+, Eu3+, Sm3+ and La3+ increased [86Rb] efflux at low concentrations in the presence of A23187, but were self inhibitory at higher concentrations. They also inhibited Ca2+-mediated [86Rb]-efflux. It is concluded that the effectiveness of a cation in activating [86Rb] efflux is, in part, related to its non-hydrated crystalline ionic radius, and that the site of activation may only accommodate ionic radii between 0.95 and 1.00 A.