1) Human B-bile was distinctly greater in antidiuretic activity than human C-bile. The b-bile was diluted with water to the extent that its bilirubin concentration equaled that of C-bile, and its antidiuretic activity was assayed in comparison with the C-bile. The diluted B-bile was found to be less potent in activity than the C-able. It was therfore thought that a part of antidiuretic substance might be reasorbed from the wall of the gall bladder. 2) Direct infusion of the biliary ADS into an isolated gall bladder of a rabbit, in which continuos diuresis had been induced, immediately lead to a cessation of urine outflow. This also indicates that the biliary ADS is reabsorbed from the gall bladder. 3) No antiduretic activity was demonstrated in human gastric juice. 4) The biliary ADS was stable in human gastric juice or C-bile. 5) The biliary ADS was resistant to pepsin treatment but was inactivated by trypsin or intestinal mucosa extract. 6) Introduction of the biliary ADS into the rat stomach or into the rabbit intestine resulted in no depression of diuresis. 7) The bilary ADS was inactivated by perfusion through an isolated rabbit liver and by rat liver extract. 8) The biliary ADS probably has the same properties as Pitressin except that the latter is stable during trypsin treatment. 9) It has been concluded that the biliary ADS is reabsorbed from the gall bladder and inactivated in the intestine. Even though it is not completely in activated in the intestine, there is no absorption from the intestinal wall. While circulating in the blood stream, it is inactivated by the liver.