Abstract
It is well known that arginine vasotocin (AVT) stimulates the sodium reabsorption by increasing the number of epithelial sodium channels (ENaC) in the apical membrane of renal epithelial cells. It is also indicated that chloride ions regulate cell functions such as cell growth and neurite elongation. However, the effect of Cl− on the AVT-stimulated ENaC-mediated current is unclear. In the present study, we examined effects of Cl− on the AVT-stimulated benzamil-sensitive currents in renal epithelial A6 cells. AVT significantly increased the benzamil-sensitive currents in A6 cells. Lowering the Cl− concentration of the apical and basolateral solutions by replacing Cl− with gluconate diminished the stimulatory action of AVT on the benzamil-sensitive current, while the replacement of Cl− with NO3− had no significant effect on the AVT action. The diminishing effect of lowering Cl− on the AVT action was observed under a low Cl− condition for the apical solution, however we did not detect the diminishing effect in a low Cl− basolateral solution. These results suggest that the apical chloride ion is a key molecule for AVT to show its stimulatory action on the ENaC-mediated sodium reabsorption in renal epithelial cells. [J Physiol Sci. 2008;58 Suppl:S70]
