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.
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