Acidification stimulates chloride and fluid absorption across frog retinal pigment epithelium
Edelman, J.L.; Lin, H.; Miller, S.S.
American Journal of Physiology 266(4 Pt 1): C946-C956
1994
ISSN/ISBN: 0002-9513 PMID: 8178967 Document Number: 438703
Radioactive tracers and a modified capacitance-probe technique were used to characterize the mechanisms that mediate Cl and fluid absorption across the bullfrog retinal pigment epithelium (RPE)-choroid. In control (HCO-3/CO-2) Ringer solution, 36Cl was actively absorbed (retina to choroid) at a mean rate of 0.34 mu-eq cntdot cm-2 cntdot h-1 (n = 34) and accounted for apprx 25% of the short-circuit current. Apical bumetanide (100 mu-M) or basal 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS; 1 mM) inhibited active Cl transport by 70 and 62%, respectively. Active Cl absorption was doubled, either by removing HCO-3 from the bathing media or by elevating CO-2 from 5 to 13%, and the increased flux was inhibited by apical bumetanide or basal DIDS. Open-circuit measurements of fluid absorption rate (J-v) and the net fluxes of 36Cl, 22Na, and 86Rb (K substitute) indicated that CO-2-induced acidification stimulated NaCl and fluid absorption across the RPE. During acidification, bumetanide produced a twofold larger inhibition of J-v compared with control. Stimulation of net Cl absorption was most likely caused by inhibition of the basolateral membrane intracellular pH-dependent Cl-HCO-3 exchanger.