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

In the intact eye, a transition from light to dark increases K concentration ([K](0)) from similar to 2 to 5 mM in the extracellular (subretinal) space between the photoreceptors and the retinal pigment epithelium (RPE) apical membrane. In control (HCO3/CO2) Ringer solution, Cl-36 was actively absorbed across isolated bullfrog RPE (retina to choroid) at a rate of 0.31 +/- 0.02 (SE) mu eq.cm(-2).h(-1) (n = 15). Elevating apical [K](0) from 2 to 5 mM reversed active Cl-36 transport to secretion (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'-diisothiocyanostilbene-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%. Apical 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], significantly inhibited [K](0), Ba2+ and low CO2-induced Cl secretion. All of these results can be understood in terms of an intracellular pH-dependent stimulation of the basolateral membrane Cl-HCO3 exchanger.