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Quarterly Journal of Experimental Physiology 73.6 pp 941-949
© The Physiological Society 1988
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EFFLUX OF CHLORIDE FROM THE RAT LENS: INFLUENCE OF MEMBRANE POTENTIAL AND INTRACELLULAR ACIDIFICATION

S. Bassnett 1, S. Stewart 2, G. Duncan 2, and P. C. Croghan 2

1 Uniformed Services University of the Health Sciences, School of Medicine, 4301 Jones Bridge Road, Bethesda, MD 20814, U.S.A.
2 School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ

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.

Submitted on February 10, 1988
Accepted on April 27, 1988




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