Potassium-induced chloride secretion across the frog retinal pigment epithelium.

In the intact eye, a transition from light to dark increases K concentration ([K]o) from approximately 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, 36Cl 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]o from 2 to 5 mM reversed active 36Cl 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]o induced a similar reversal of net 36Cl flux and inhibited fluid absorption by approximately 25%. Apical Ba2+ (1 mM), decreased CO2 (5 to 1%), or increased apical bath HCO3 concentration ([HCO3]o) also caused a DIDS-inhibitable reversal of active 36Cl flux. A 10-fold reduction of apical bath Na or [HCO3]o significantly inhibited [K]o, 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.