Model of ionic transport for bovine ciliary epithelium: effects of acetazolamide and HCO 3 −

The possible existence of transepithelial bicarbonate transport across the isolated bovine ciliary body was investigated by employing a chamber that allows for the measurement of unidirectional, radiolabeled fluxes of CO2 + HCO[Formula: see text]. No net flux of HCO[Formula: see text] was detected. However, acetazolamide (0.1 mM) reduced the simultaneously measured short-circuit current ( I sc). In other experiments in which36Cl− was used, a net Cl− flux of 1.12 μeq · h−1 · cm−2 (30 μA/cm2) in the blood-to-aqueous direction was detected. Acetazolamide, as well as removal of HCO[Formula: see text] from the aqueous bathing solution, inhibited the net Cl− flux and I sc. Because such removal should increase HCO[Formula: see text] diffusion toward the aqueous compartment and increase the I sc, this paradoxical effect could result from cell acidification and partial closure of Cl−channels. The acetazolamide effect on Cl− fluxes can be explained by a reduction of cellular H+ and HCO[Formula: see text] (generated from metabolic CO2production), which exchange with Na+ and Cl−via Na+/H+ and Cl−/HCO[Formula: see text] exchangers, contributing to the net Cl− transport. The fact that the net Cl−flux is about three times larger than the I sc is explained with a vectorial model in which there is a secretion of Na+ and K+ into the aqueous humor that partially subtracts from the net Cl− flux. These transport characteristics of the bovine ciliary epithelium suggest how acetazolamide reduces intraocular pressure in the absence of HCO[Formula: see text] transport as a driving force for fluid secretion.