Abstract
Na+channel activity in cultured renal (A6) epithelium is regulated by the solution osmolarity. In the present study we examined which pathway downstream of PLA2 is involved. A6 cells were grown on permeable supports and mounted into a water-jacketed (28°C) Ussing chamber. Transepithelial electrical measurements were made under open circuit conditions. The transepithelial conductance (Gt) was determined by pulsed current injections (ΔI =1μA) and Isc was calculated. A hypo-osmotic shock (from 260 to 160 mosm/kg H2O) was induced after an equilibration period of 30 minutes by decreasing the NaCl concentration of the mucosal and serosal solutions. After 40 minutes exposure to hypotonicity the Isc increased from 1.6±0.3 μA/cm2 to 9.3±2.2 μA/cm2 (n=8). In the presence of the PLA2 blocker quinacrine (100 μmol/l) Isc hardly increased from 1.9±0.4 μA/cm2 to 2.2±0.6 μA/cm2 (n=4). The Ca2+-insensitive PLA2 blocker bromoenol lactone (10 μmol/l), the COX-1 inhibitor resveratrol (10 μmol/l), and the COX-2 inhibitor celecoxib (20 μmol/l) did not inhibit the hypo-induced increase in Isc. In the presence of the 5-lipoxygenase inhibitor nordihydroguaiaretic acid (20 μmol/l) Isc increased only from 2.4±0.3 μA/cm2 to 6.5±1.3 μA/cm2 (n=6). The data suggest that the leukotriene pathway might contribute to the osmotic regulation of sodium channel activity in A6 cells.
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