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Mechanism of Control of Adrenocorticotrophic Hormone *

W. McDermott,E. G. Fry,J. Brobeck,C. Long

Published 1950 in The Yale Journal of Biology and Medicine

ABSTRACT

Experiments indicating that epinephrine activates the adrenal cortex only when the pituitary gland is intacte"" have led to the suggestion that epinephrine may exert an action directly upon the secretory cells of the anterior hypophysis." At the same time, a number of other drugs, notably histamine,' have also been shown to bring about the release of ACTH, and this finding has tended to relegate epinephrine to the role of a nonspecific agent in the activation mechanism. This is true particularly since a series of reports published by Sayers and his associates' have demonstrated that the output of adrenocorticotrophic hormone is suppressed when the level of adrenal cortical hormones rises in the circulating blood-an observation which has suggested that the level of circulating cortical hormones controls the ACTH output of the pituitary in much the same manner that the level of estrogens influences the output of the follicle stimulating hormone. It may be noted, however, that histamine as well as many other drugs which stimulate the release of ACTH are known to cause also a rapid release of epinephrine from the adrenal medulla," so that the possibility remains that a variety of other drugs may exert their action through the epinephrine mechanism. Since stating the original hypothesis concerning the role of epinephrine in activating the pituitary-adrenal system,' Long and his associates have continued to study the specificity of the response and the mechanisms through which it is brought about. Their data appear to show that epinephrine does not activate the pituitary through any of its other metabolic actions on electrolyte or carbohydrate metabolism. While they confirm, in part, the work of Sayers and his colleagues, the data of Long, et al.," and of McDermott, et al.," suggest that epinephrine has a specific role and an action directly upon the pituitary gland. In order to attempt a correlation of the data available on the mechanisms controlling the secretion of ACTH, and to investigate further the role of epinephrine in this control, it seemed necessary to compare normal animals with animals which were unable to liberate endogenous epinephrine in

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