BASOLATERAL POTASSIUM MEMBRANE-PERMEABILITY OF A6 CELLS AND CELL-VOLUME REGULATION

The K+ permeabilities (Rb-86(K) transport) of the basolateral membrane s (J(b)K) of a renal cell line (A6) were compared under isosmotic and hypo-osmotic conditions (serosal side) to identify the various compone nts involved in cell volume regulation. Changing the serosal solution to a hypo-osmotic one (165 mOsm) induced a fast transient increase in Ca-i (max <1 min) and cell swelling (max at 3-5 min) followed by a reg ulatory volume decrease (5-30 min) and rise in the SCC (stabilization at 30 min). In isosmotic conditions (247 m0sm), the Rb-86(K) transport and the SCC were partially blocked by Ba2+, quinidine, TEA and gliben clamide, the latter being the least effective. Changing the osmolarity from isosmotic to hypo-osmotic resulted in an immediate (within the f irst 3-6 min) stimulation of the Rb-86(K) transport followed by a prog ressive decline to a stable value higher than that found in isosmotic conditions. A serosal Ca2+-free media or quinidine addition did not af fect the initial osmotic stimulation of J(b)K but prevented its ''seco ndary regulation,'' whereas TEA, glibenclamide and DIDS completely blo cked the initial J(b)K increase. Under hypo-osmotic conditions, the in itial J(b)K increase was enhanced by the presence of 1 mM of barium an d delayed with higher concentrations (5 mM). In addition, cell volume regulation was fully blocked by quinidine, DIDS, NPPB and glibenclamid e, while partly inhibited by TEA and calcium-free media. We propose th at a TEA- and glibenclamide-sensitive but quinidine-insensitive increa se in K+ permeability is involved in the very first phase of volume re gulation of A6 cells submitted to hypo-osmotic media. In achieving cel l volume regulation, it would play a complementary role to the quinidi ne-sensitive K+ permeability mediated by the observed calcium rise.