Amiloride stimulation of sodium transport in the presence of calcium and a divalent cation chelator.

Amiloride in nM to microM concentrations stimulates the short circuit current (Isc) of the toad urinary bladder by as much as 120% when applied in conjunction with apical Ca2+ and a divalent cation chelator. A significant decrease in transepithelial resistance (Rt) is observed simultaneously. This response is spontaneously reversible and its amplitude is dependent upon apical sodium concentrations. The stimulated Isc persisted when acetazolamide (1 mM) was introduced, HPO2-4 substituted for HCO-3 or SO2-4 replaced Cl-. Consequently, the increase in Isc is not due to the change of Cl-, H+ or HCO-3 flux. This behavior in a 'tight' epithelium may be related to the mechanism controlling apical sodium permeability.