SINCE the classical demonstration by Long and Sayers and their coworkers (cf. 1–3) that adrenal ascorbic acid levels were acutely depleted under conditions of enhanced adrenal cortical activity, the fate of the vitamin disappearing and its role in the production, secretion and utilization of the corticosteroids have been the subject of extensive inquiry (cf. 4, 5). Only Vogt (6) appears to have investigated directly the possibility that the ascorbic acid lost by the adrenal gland under these circumstances might be secreted into the adrenal vein. However, she was unable to demonstrate a consistent secretion of this vitamin into the adrenal venous effluent of the dog even after splanchnic stimulation. The release of ascorbic acid into the perfusion fluid by adrenal glands in vitro has been noted by Heard and Welch (7) and Rosenfeld (8). Peripheral plasma levels of ascorbic acid have been observed to rise following prolonged bleeding (1) and splanchnic stimulation (9) in the rat and ACTH administration in man (10). However, the contribution of the adrenal gland to this increase has not been determined.