Regulatory volume decrease after exposure to hypo-osmotic media in MDCK epithelial cells results from activation of both K+ and Cl- conductances. Swelling-stimulated 86Rb(K) losses were observed only across the basal-lateral membrane and were relatively insensitive to 10 mM Ba2+. The effect of hypo-
The effect of hyperosmotic challenge upon ion transport in cultured renal epithelial layers (MDCK)
โ Scribed by N. L. Simmons; D. R. Tivey
- Publisher
- Springer
- Year
- 1992
- Tongue
- English
- Weight
- 852 KB
- Volume
- 421
- Category
- Article
- ISSN
- 0031-6768
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โฆ Synopsis
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 adrenalinestimulated inward short-circuit current (C1-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 CI-cotransporter at the basal-lateral membranes was markedly stimulated by hypertonic exposure. A diuretic-sensitive K+(C1 -) loss was observed in shrunken cells upon prolonged exposure (20 rain), showing that the net direction of "cotransport" flux was outward. 86Rb(K+) efflux stimulated by adrenaline (100gM), exogenous ATP (100 gM) and A23187 (10 gM) 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.
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