The effect of hyperosmotic challenge upon ion transport in cultured renal epithelial layers (MDCK).

Exposure of the basal-lateral surfaces of MDCK epithelia, mounted in Ussing chambers, to medium made hyperosmotic by the non-electrolyte mannitol, resulted in a marked inhibition of the adrenaline-stimulated inward short-circuit current (Cl- secretion). This inhibition was unaccompanied by a reversal of the adrenaline-stimulated increment in tissue conductance, indicating that the inhibition was due to modulation of ion transport at the basal-lateral membranes. Loop-diuretic-sensitive 86Rb(K+) efflux mediated by the Na+ - K+ -2 Cl- cotransporter at the basal-lateral membranes was markedly stimulated by hypertonic exposure. A diuretic-sensitive K+ (Cl-) loss was observed in shrunken cells upon prolonged exposure (20 min), showing that the net direction of "cotransport" flux was outward. 86Rb(K+) efflux stimulated by adrenaline (100 microM), exogenous ATP (100 microM) and A23187 (10 microM) was attenuated in shrunken cells, suggesting that basal-lateral K+ conductance is reduced in hyperosmotic media. "Cotransport" stimulation by hyperosmotic medium was asymmetric, apical bathing hypertonicity being ineffective. These data are consistent with a low hydraulic permeability of the apical membranes.