Chloride is required for fluid transport by the rabbit corneal endothelium.

Abstract

The role of chloride in fluid transport of the rabbit corneal endothelium was examined by measuring changes in corneal thickness following ion substitutions or addition of ion transport inhibitors in media superfusing the isolated tissue. Normal fluid transport is indicated by maintenance of constant thickness in a fresh cornea or thinning (deturgescence) of a preswollen deepithelialized cornea to its initial thickness at approximately 40 microns/h. These patterns are seen when tissues are superfused with HCO(3-)-Ringer containing 114 mM Cl-. When Cl- was substituted with gluconate, glucuronate, or SO4(2-) fresh and preswollen corneas immediately thinned at greater than 150 microns/h to a value less than 300 microns and then began to swell at 30 microns/h to above their original thickness. Substitution of Cl- with NO3- or Br- had a negligible immediate thinning effect, but fresh corneas subsequently swelled and preswollen corneas failed to deturgesce fully. The rapid thinning (called a "downtransient") observed with gluconate, glucuronate, and SO4(2-) also occurred in these media when ion and fluid transport were completely inhibited with ouabain or stilbenes or by absence of HCO3-, indicating that the thinning results from osmotic gradients induced by ionic reflection coefficients different from that of Cl-. When the downstransient was avoided in deepithelialized corneas by preswelling with the same Cl(-)-free media on both sides of the cornea, corneas maintained a constant but swollen thickness in gluconate and in NO3- or Br- deturgesced slowly and incompletely; ouabain or stilbenes caused further swelling in all media. We conclude that absence of Cl- partially impairs fluid transport, most probably via its role in a Cl(-)-HCO3- exchanger which has been proposed in a recent model of endothelial fluid transport.