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Structure-activity studies on the corticosteroid fast and delayed feedback receptor mechanisms controlling the secretion of corticotrophin releasing factor (CRF) were carried out with the rat hypothalamus in vitro. The secretion of CRF was induced by acetylcholine (3 pg/ml). The fast feedback receptor appears highly specific, and the structure essential for efficacy involves an 11beta-hydroxyl group and an unblocked 21-hydroxyl group. Several steroids showed antagonism and so the binding site is not very specific. 18-hydroxy, 11-deoxycorticosterone, progesterone, 17alpha-hydroxyprogesterone and 11-deoxycorticosterone were antagonists of fast feedback. The delayed feedback receptor required either an 11beta-or a 21-hydroxyl group for efficacy. The binding site required a 17-hydroxyl group when the 11beta- or 21-hydroxyl groups were absent. Binding also involved the 3-oxo,4,5-ene structure since steroids in which these are absent were inactive.
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