The possible existence of transepithelial bicarbonate transport across the
isolated bovine ciliary body was investigated by employing a chamber that a
llows for the measurement of unidirectional, radiolabeled fluxes of CO2 + H
CO3-. No net flux of HCO3- was detected. However, acetazolamide (0.1 mM) re
duced the simultaneously measured short-circuit current (Isc). In other exp
eriments in which Cl-36(-) was used, a net Cl- flux of 1.12 mu eq.h(-1).cm(
-2) (30 muA/cm(2)) in the blood-to-aqueous direction was detected. Acetazol
amide, as well as removal of HCO3- from the aqueous bathing solution, inhib
ited the net Cl- flux and I-sc. Because such removal should increase HCO3-
diffusion toward the aqueous compartment and increase the I-sc, this parado
xical effect could result from cell acidification and partial closure of Cl
- channels. The acetazolamide effect on Cl- fluxes can be explained by a re
duction of cellular H+ and HCO3- (generated from metabolic CO2 production),
which exchange with Na+ and Cl- via Na+/H+ and Cl-/HCO3- exchangers, contr
ibuting to the net Cl- transport. The fact that the net Cl- flux is about t
hree times larger than the I-sc is explained with a vectorial model in whic
h 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 bov
ine ciliary epithelium suggest how acetazolamide reduces intraocular pressu
re in the absence of HCO3- transport as a driving force for fluid secretion
.