We compared the effects exerted by two classes of Cl transport inhibitors on a Cl-selective, passive anion transport route across the skin of Bufo viridis, the conductance (G_Cl) of which can be activated by transepithelial voltage perturbation or high cAMP at short circuit. Inhibitors of antiporters (erythrosine, eosin) or cotransporters (furosemide) reduced voltage-activated G_Cl with IC₅₀ of 6 ± 1, 54 ± 12, and 607 ± 125 µM, respectively; they had no effect on the cAMP-induced G_Cl. The voltage for half-maximal activation of G_Cl (V₅₀) increased compared with controls, but effects on the maximal G_Cl at more positive clamp potentials were small. Cl channel blockers from the diphenylamino-2-carboxylic acid (DPC) family [dichloro-DPC, niflumic acid, flufenamic acid, and 5-nitro-2-(3-phenylpropylamino)benzoic acid] reduced the voltage-activated G_Cl with IC₅₀ of 8.3 ± 1.2, 10.5 ± 0.6, 16.5 ± 3.4, and 36.5 ± 11.4 µM, respectively, and also inhibited the cAMP-induced G_Cl, albeit with slightly larger IC₅₀. V₅₀ was not significantly changed compared with controls; the maximal G_Cl was strongly reduced. We conclude that the pathway for Cl is composed of the conductive pore proper, which is blocked by the derivatives of DPC, and a separate, voltage-sensitive regulator, which is influenced by blockers of cotransporters or antiporters. This influence is partly overcome by increasing the clamp potential and removed by high concentrations of cAMP, which renders the pathway insensitive to voltage.