POTASSIUM-INDUCED CHLORIDE SECRETION ACROSS THE FROG RETINAL-PIGMENT EPITHELIUM

In the intact eye, a transition from light to dark increases K concent ration ([K](0)) from similar to 2 to 5 mM in the extracellular (subret inal) space between the photoreceptors and the retinal pigment epithel ium (RPE) apical membrane. In control (HCO3/CO2) Ringer solution, Cl-3 6 was actively absorbed across isolated bullfrog RPE (retina to choroi d) at a rate of 0.31 +/- 0.02 (SE) mu eq.cm(-2).h(-1) (n = 15). Elevat ing apical [K](0) from 2 to 5 mM reversed active Cl-36 transport to se cretion (choroid to retina), with a rate of 0.76 +/- 0.17 mu eq.cm(-2) .h(-1). This reversal was completely inhibited by 1 mM 4,4'-diisothioc yanostilbene-2,2'-disulfonic acid (DIDS) in either the apical or basal bath. In open circuit, elevating [K](0) induced a similar reversal of net Cl-36 flux and inhibited fluid absorption by similar to 25%. Apic al Ba2+ (1 mM), decreased CO2 (5 to 1%), or increased apical bath HCO3 concentration ([HCO3](0)) also caused a DIDS-inhibitable reversal of active Cl-36 flux. A 10-fold reduction of apical bath Na or [HCO3], si gnificantly inhibited [K](0), Ba2+ and low CO2-induced Cl secretion. A ll of these results can be understood in terms of an intracellular pH- dependent stimulation of the basolateral membrane Cl-HCO3 exchanger.