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Abstract

The rate of valinomycin-induced KCl efflux from human red cells and ghosts was measured in the presence and absence of phlorizin. Extracellular phlorizin accelerated the KCl efflux. The effect depended on the phlorizin concentration and showed half saturation at about 0.4mM phlorizin. Hunter's procedure was used to calculate Cl permeabilities (P _Cl) by means of the Goldman equation from rate constants of K⁺ loss in valinomycin-treated ghosts. For saturating phlorizin concentrations a 20-fold increase, approximately, ofP _Cl was calculated. The observed increase inP _Cl is in contrast to the almost total inhibition of Cl⁻ equilibrium exchange. Similar to the effects on anion exchange permeability the effect onP _Cl is only observed when phlorizin is present at the outer surface of the erythrocyte membrane while internal phlorizin is without effect. A similar asymmetry was observed in the stimulation of valinomycin-induced K⁺ exchange at identical K⁺ concentrations on both sides of the membrane. The effects of phlorizin were only observed if net KCl flow was out of the cells but not if it was in the opposite direction. The effect of phlorizin on net KCl movements and sugar transfer were unaltered when the phlorizin was subjected to several consecutive purifications. This indicates that the observed effects are due to the glycoside and not to contaminations with its aglycone.