The Steroid Feedback Mechanism

¹ From the Institute for Medical Research, Cedars of Lebanon Hospital, Los Angeles, California

The mechanism whereby high blood levels of the adrenal cortical hormones inhibit the secretion of ACTH following stress has been investigated. The 4-hour change in circulating eosinophils was used as criterion for ACTH secretion. DCA administration into intact rats prevented the endogenous mobilization of ACTH following stress. When the venous brain blood from the stressed hypophysectomized rat was injected into these DCA-treated intact rats, a discharge of ACTH occurred in the recipients as indicated by a pronounced 4-hour eosinopenia. Carotid artery blood from stressed hypophysectomized rats was relatively inactive in provoking ACTH secretion when injected into intact DCA-treated recipients. If DCA is administered to the hypophysectomized donor rat, its brain blood contains no, or only slight, pituitary stimulating activity. It is concluded that at least one mechanism whereby high levels of the adrenal cortical hormones inhibit the release of ACTH following stress is by blocking the secretion from a cerebral structure, presumably the hypothalamus, of a pituitary stimulating substance (s).