Abstract
IN 1908, Babes and Jonescu observed that conditions of stress in man and laboratory animals were associated with the depletion of suprarenal lipid. Multiple intravenous injections of epinephrine produced a similar depletion, accompanied by adrenal hypertrophy in rabbits (1). Vogt later demonstrated that following the administration of epinephrine, cortical hormones could be detected in the adrenal venous blood of cats and dogs (2). Long and Fry (3) studied this response of the adrenal cortex to epinephrine, using the assay of Sayers (4) for adrenal corticotropic hormone (ACTH). They described a significant ACTH release in response to injected epinephrine in normal rats; on the other hand, hypophysectomized rats failed to show this response, in spite of the fact that their adrenal cortices were maintained with exogenous pituitary hormone injections. From these data Long postulated that the effect of epinephrine on the adrenal cortex was mediated by the pituitary. Vogt subsequently reported similar differen...
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