Abstract

Normal vision depends, in part, on the combined refractive powers of the cornea and crystalline lens to permit adequate focusing of light onto the retina. Such refractive function requires that the cornea remain transparent, a requirement that is met provided that corneal hydration, i.e., deturgescence, is maintained within specific physiological limits. Maintenance of corneal deturgescence is reliant upon coupled ion and fluid transport activities within the epithelial and endothelial layers. Net ion transport activity offsets the natural tendency of the corneal stroma to imbibe fluid from the anterior chamber, thus keeping the cornea transparent (1–5). Although most of the ion transport activity involved in maintaining corneal deturgescence is contingent upon ion transport processes localized in the corneal endothelial layer, corneal epithelial ion transport activity plays a fine-tuning role in maintaining corneal deturgescence during exposure to environmental challenges (6) (Fig. 1). Only under maximally stimulated conditions is the epithelial-side fluid transport rate able to increase sufficiently, i.e., to approximately 25% of the endothelial-side fluid transport rate (7). This realization has prompted a host of studies concentrated on characterizing receptor-mediated regulation of corneal epithelial active ion transport.

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