Two types of K+ currents modulated by arachidonic acid in bovine corneal epithelial cells.

PURPOSE

Fenamate sensitivity of the large-conductance K+ current in the corneal epithelium suggests that K+ transport could be modulated by arachidonic acid (AA) and/or its metabolites, which also regulate corneal epithelial migration. The main purpose of this study was to investigate AA-induced modulation of K+ currents expressed in the bovine corneal epithelium.

METHODS

Freshly isolated bovine corneal epithelial cells were perfused with Ringer solution. Whole-cell currents were recorded by using either the conventional whole-cell-patch or the perforated-patch configuration.

RESULTS

Two distinct types of K+ currents dominated the whole-cell current. The first was a voltage-gated K+ current that was inactivated completely by membrane depolarization. The inactivating voltage-gated K+ current was largest in presumptive basal cells. The second was a noisy, sustained K+ current that was never inactivated and seemed to be a counterpart of the large-conductance K+ current reported in the rabbit corneal epithelium. External application of AA (5-20 microm) inhibited the inactivating voltage-gated K+ current and augmented the noisy, sustained K+ current. Identical dual modulation was induced by other fatty acids (e.g., palmitoleic acid) that are not substrates for enzymes in the AA cascade.

CONCLUSIONS

An inactivating voltage-gated K+ channel was identified for the first time in the corneal epithelium. AA and some fatty acids may directly activate the large-conductance K+ channel to augment its housekeeping functions in corneal epithelial cells.