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Am J Physiol Cell Physiol 277: C545-C553, 1999;
0363-6143/99 $5.00
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Vol. 277, Issue 3, C545-C553, September 1999

Apical and basolateral CO2-HCOminus 3 permeability in cultured bovine corneal endothelial cells

Joseph A. Bonanno1, Yi Guan2, Sergey Jelamskii1, and Xiao Jun Kang2

1 School of Optometry, Indiana University, Bloomington, Indiana 47401; and 2 School of Optometry, University of California, Berkeley, California 94720

Corneal endothelial function is dependent on HCO-3 transport. However, the relative HCO-3 permeabilities of the apical and basolateral membranes are unknown. Using changes in intracellular pH secondary to removing CO2-HCO-3 (at constant pH) or removing HCO-3 alone (at constant CO2) from apical or basolateral compartments, we determined the relative apical and basolateral HCO-3 permeabilities and their dependencies on Na+ and Cl-. Removal of CO2-HCO-3 from the apical side caused a steady-state alkalinization (+0.08 pH units), and removal from the basolateral side caused an acidification (-0.05 pH units). Removal of HCO-3 at constant CO2 indicated that the basolateral HCO-3 fluxes were about three to four times the apical fluxes. Reducing perfusate Na+ concentration to 10 mM had no effect on apical flux but slowed basolateral HCO-3 flux by one-half. In the absence of Cl-, there was an apparent increase in apical HCO-3 flux under constant-pH conditions; however, no net change could be measured under constant-CO2 conditions. Basolateral flux was slowed ~30% in the absence of Cl-, but the net flux was unchanged. The steady-state alkalinization after removal of CO2-HCO-3 apically suggests that CO2 diffusion may contribute to apical HCO-3 flux through the action of a membrane-associated carbonic anhydrase. Indeed, apical CO2 fluxes were inhibited by the extracellular carbonic anhydrase inhibitor benzolamide and partially restored by exogenous carbonic anhydrase. The presence of membrane-bound carbonic anhydrase (CAIV) was confirmed by immunoblotting. We conclude that the Na+-dependent basolateral HCO-3 permeability is consistent with Na+-nHCO-3 cotransport. Changes in HCO-3 flux in the absence of Cl- are most likely due to Na+-nHCO-3 cotransport-induced membrane potential changes that cannot be dissipated. Apical HCO-3 permeability is relatively low, but may be augmented by CO2 diffusion in conjunction with a CAIV.

bicarbonate permeability; epithelial transport; carbonic anhydrase


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