In the accompanying paper, a compartmental model for the toad bladder sodium transport system was developed. In the present paper, the model is tested by determining the effects of antidiuretic hormone on the pools and fluxes. It is shown that this hormone affects only that sodium pool previously designated as the transport pool, and that the effects are on two separate sites. In the first place, the hormone stimulates entry at the mucosal side of the transport compartment, and by this means brings about an increase in the amount of sodium contained in the compartment. Second, the hormone has a distinct stimulatory effect on the rate coefficient for efflux across the serosal boundary, the pump rate coefficient. Evidence is presented that under control conditions, the pump rate coefficient is a decreasing function of the pool size, a characteristic feature of a saturating system. Therefore, the effect of vasopressin in increasing both the pool size and the pump rate coefficient must be construed as a direct effect on the pump, and not one which is secondary to the increase in the pool size. Furthermore, it is shown that the effect of the hormone on the sodium pump is not dependent on the presence of sodium in the serosal medium.In the accompanying paper (Finn and Rockoff, 1971) it was shown that it is possible to represent toad bladder sodium content by a compartmental model. It was found that a system containing two noncommunicating tissue compartments satisfied the data obtained from the washout of radioactive sodium, and that one of these compartments was quite likely to be the transport pool. However, in order to establish more firmly that such a model is biologically relevant, it is necessary to demonstrate that biological perturbations affect the system in a consistent and reasonable manner. In the present paper, we explore the effects of antidiuretic hormone on these transport parameters. In addition, some of the effects of changes in the sodium concentration in the media will be examined.