Neurohypophyseal hormones are known to affect the transfer characteristics of some amphibian epithelia to salt and water. The general view of sodium transport across toad bladder is that sodium enters the cells passively down a concentration gradient from the mucosal solution, and is pumped into the serosal solution by an unsaturated ion pump. Neurohypophyseal hormones are believed to stimulate transport by increasing the permeability of the mucosal surface to sodium ions. Measurements of the amount of sodium in the transport pool by tissue pool labelling has shown that the electrochemical gradient may not always be favourable for sodium entry across the mucosal border. Furthermore, other experiments have demonstrated that most of the labelled sodium pool, presumably intracellular, is beyond the active transport step. These difficulties have led to suggestions of alternative models for the active transport of sodium and for the actions of neurohypophyseal peptides. In this paper the effects of amiloride on short circuit current and sodium fluxes in isolated toad bladder is described, and an alternative view of the transport process is suggested.