EFFLUX OF CHLORIDE FROM THE RAT LENS: INFLUENCE OF MEMBRANE POTENTIAL AND INTRACELLULAR ACIDIFICATION

Abstract

The efflux of ³⁶Cl⁻ from perifused rat lenses consisted of two components: a fast (extracellular) component and a slow (cellular) component. The ³⁶Cl⁻ efflux rate constant of the cellular component was 5·7 x 10⁻³ min⁻¹. The ³⁶Cl⁻ efflux was sensitive to changes in lens potential induced by treatment with high‐K⁺ solutions. The decrease in the ³⁶Cl⁻ efflux rate constant caused by high‐K⁺ solutions was consistent with the Goldman model, indicating that, under normal conditions, the majority of the ³⁶Cl⁻ efflux is by diffusion. The ³⁶Cl⁻ efflux rate constant corresponds to a Cl⁻ permeability of 1·3 x 10⁻⁸ m s⁻¹. The Cl⁻ channel inhibitor anthracene‐9‐carboxylate (A‐9‐C), however, caused a relatively small reduction in the efflux rate constant. The anion‐exchange inhibitor 4‐acetamido‐4'‐isothiocyanatostilbene‐2,2'‐disulphonate (SITS) has little effect on the ³⁶Cl⁻ efflux under control conditions. Intracellular acidification, induced by pre‐treatment with NH₄⁺, leads to a rapid stimulation of ³⁶Cl⁻ efflux. This increased ³⁶Cl⁻ efflux is blocked by SITS. Thus, it appears that at low intracellular pH (pH_i), a normally quiescent, SITS‐sensitive, anion‐exchange mechanism is activated. The possible role of this exchange mechanism in regulating pH_i is discussed.