Responses of Adrenal Corticosteroid Secretion to

that hemorrhage leads to depletion of adrenal ascorbic acid through a mechanism dependent on the pituitary and presumably involving the re-lease of ACTH (1). Hume and Nelson pre-sented evidence that hemorrhage was effective in increasing secretion of 17-hydroxycorticosteroids (17-OHCS) and that this effect was dependent upon the pituitary (2). Subsequent reports have confirmed (3-5) or failed to confirm (6, 7) these observations without, however, extending our un-derstanding of the mechanism by which hemor-rhage stimulates release of ACTH and secretion of 17-OHCS. The present experiments repre-sent a first attempt to define these mechanisms. Method