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.
D000818:Animals; D001693:Biological Transport, Active; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D002460:Cell Line; D004232:Diuretics / Q000494:pharmacology; D004285:Dogs; D004837:Epinephrine / Q000494:pharmacology; D004847:Epithelial Cells; D004848:Epithelium / Q000378:metabolism; D006982:Hypertonic Solutions; D007473:Ion Channels / Q000187:drug effects*; D007668:Kidney / Q000166:cytology / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects; D012414:Rubidium Radioisotopes
D004232:Diuretics; D006982:Hypertonic Solutions; D007473:Ion Channels; D015221:Potassium Channels; D012414:Rubidium Radioisotopes; D000001:Calcimycin; D002118:Calcium; D004837:Epinephrine