APICAL MEMBRANE SODIUM AND CHLORIDE ENTRY DURING OSMOTIC SWELLING OF RENAL (A6) EPITHELIAL-CELLS

To assess the role of chloride in cell volume and sodium transport reg ulation, we measured cell height changes (CH), transepithelial chlorid e and sodium fluxes, and intracellular chloride content during challen ge with hyposmotic solutions under open circuit (OC) conditions. CH ma ximally increased following hyposmotic challenge within similar to 5 m inutes. The change in CH was smaller under short circuit (SC) conditio ns or following replacement of chloride in the mucosal solution by glu conate or cyclamate (Cl--free(m)). When corrected for the osmotically inactive cell volume (30 +/- 2%), Delta CH for controls (OC) were grea ter than predicted for an ideal osmometer. In contrast, Delta CH for C T(-)free(m) or SC conditions were similar to that predicted for an ide al osmometer. Na+ and Cl- mucosa-to-serosa fluxes increased following hyposmotic challenge. Chloride fluxes increased maximally within 5 min , then decreased. In contrast, the Na+ flux increased slowly and reach ed a steady state after similar to 25 min. Under isosmotic conditions, exposure to Cl--free(m) solutions led to decreases in the transepithe lial conductance, Na+ flux, and CH. Chloride permeabilities in the api cal and basolateral membranes were detected using the fluorescent intr acellular chloride indicator MQAE. The results indicate that during os motic swelling, the entry of both sodium and chloride is increased. Th e time courses of these increases differ, suggesting distinct mechanis ms for the osmotic regulation of these apical membrane transport proce sses.