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

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.