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The effect of hypo-osmolarity upon transepithelial ion transport in cultured renal epithelial layers (MDCK)

โœ Scribed by N. L. Simmons


Publisher
Springer
Year
1991
Tongue
English
Weight
756 KB
Volume
419
Category
Article
ISSN
0031-6768

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โœฆ Synopsis


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-osmotic media upon MDCK epithelia mounted in Ussing chambers has been investigated. Exposure of the basal-lateral surfaces to hypo-osmotic media resulted in a transient stimulation of inward short-circuit current (Isc) followed by inhibition of inward Isc in both control layers and in layers where inward current (due to transepithelial Cl- secretion) was first stimulated by 5 microM prostaglandin E1 (PGE1). The transient stimulation of inward current by hypo-osmotic media was not markedly attenuated by 10 mM Ba2+ in PGE1-stimulated layers. After stimulation of inward (Cl(-)-secretory) current to high levels by 10 microM adrenaline, the predominant effect of basal-lateral exposure to hypo-osmotic media was an inhibition of the inward current. This inhibition was partially reversed by 40 microM 4,4'-diisothiocyanatostilbene-2,2'-disulphonate (DIDS). The stimulation, then inhibition, of inward Isc is likely to be the result of separate swelling-induced K+ and Cl- conductances (respectively) at the basal-lateral membrane. The swelling-stimulated Cl- conductance is distinct from the apical Cl- conductance regulated by PGE1 or adrenaline.


๐Ÿ“œ SIMILAR VOLUMES


The effect of hyperosmotic challenge upo
โœ N. L. Simmons; D. R. Tivey ๐Ÿ“‚ Article ๐Ÿ“… 1992 ๐Ÿ› Springer ๐ŸŒ English โš– 852 KB

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