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 (pHi), a normally quiescent, SITS‐sensitive, anion‐exchange mechanism is activated. The possible role of this exchange mechanism in regulating pHi is discussed.