Vasopressor and oxytocic activities were detectable in the pars nervosa of mice with hereditary diabetes insipidus (DI Os/+ strain). This finding shows that the diabetes insipidus of DI mice is due to a primary defect of the kidney and not to vasopressin deficiency. Both activities of the DI mice were significantly higher than in normal mice (VII +/+) when the activities were expressed in terms of the individual. However, when the activity was expressed per mg of dry weight of the pars nervosa, the difference in oxytocic activity of the two groups seemed to be no longer significant, although vasopressor activity was still greater in the DI mice.