Model of ionic transport for bovine ciliary epithelium: effects of acetazolamide and HCO
CH To, CW Do, AC Zamudio… - American Journal of …, 2001 - journals.physiology.org
CH To, CW Do, AC Zamudio, OA Candia
American Journal of Physiology-Cell Physiology, 2001•journals.physiology.orgThe 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 3−. No net flux of HCO 3− 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 …
ciliary body was investigated by employing a chamber that allows for the measurement of
unidirectional, radiolabeled fluxes of CO2+ HCO 3−. No net flux of HCO 3− 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 …
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. No net flux of HCO 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 from the aqueous bathing solution, inhibited the net Cl− flux andI sc. Because such removal should increase HCO 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 (generated from metabolic CO2production), which exchange with Na+ and Cl−via Na+/H+ and Cl−/HCO 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 transport as a driving force for fluid secretion.
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