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With the introduction of the countercurrent hypothesis (1) to explain renal concentrating ability there has been renewed interest in the role of urea in renal tubular function. Recent studies (2-5) suggest that urea makes a major contribution to the urinary concentrating mechanism. If this is the case, one might expect important differences in the permeability of the renal tubule to urea in the presence or absence of antidiuretic hormone. Further, such movement of urea across the tubule might be passive, or effected by means of an active transport system, such as has been described for the bull frog kidney (6-8). The difficulty of exploring such problems in the intact mammalian kidney need not be emphasized. It would be desirable to use a simpler system, in which the movement of urea across living cells could be measured directly. The studies of Ussing, Zerahn, Koefoed-Johnsen, and Andersen (9-12) have demonstrated the usefulness of isolated, surviving amphibian membranes as models for the study of active transport and other membrane phenomena. In the studies reported below we have used the toad bladder, a tissue that resembles the mammalian renal tubule in several respects (13).

THE EFFECT OF NEUROHYPOPHYSEAL HORMONES ON THE PERMEABILITY OF THE TOAD BLADDER TO UREA*