Abstract
Amiloride in nM to μM concentrations stimulates the short circuit current ( I sc ) of the toad urinary bladder by as much as 120% when applied in conjunction with apical Ca 2+ and a divalent cation chelator. A significant decrease in transepithelial resistance ( R t ) is observed simultaneously. This response is spontaneously reversible and its amplitude is dependent upon apical sodium concentrations. The stimulated I sc persisted when acetazolamide (1 mM) was introduced, HPO 4 2− substituted for HCO 3 − or SO 4 2− replaced Cl −. Consequently, the increase in I sc 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.
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