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 ( Isc). 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 Isc. Because such removal should increase HCO[Formula: see text] diffusion toward the aqueous compartment and increase the Isc, 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 Iscis 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.