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Summary Both the circadian and stress‐induced changes in plasma corticosterone concentration were abolished by the inclusion of betamethasone in the drinking water of rats. Adrenal sensitivity to exogenous corticotrophin (ACTH) was unimpaired by the betamethasone treatment. The normal circadian rhythm in plasma corticosterone returned within 1 day of withdrawal of the steroid, but the response to stress was normal only after 3 days. The possible significance of these observations is discussed.

Summary1. Betamethasone caused growth retardation, adrenal atrophy and impaired hypothalamo-pituitary-adrenal (HPA) activity in the rat. 2. In spite of the profound impairment, recovery of normal HPA function was rapid, but the growth retardation persisted.3. The ability of the pituitary gland to secrete basal corticotrophin (ACTH), recovered more rapidly and the adrenocorticotrophic response to stress less rapidly than the ability of the adrenal cortex to respond to ACTH. 4. The degree of HPA suppression was not determined by the total dose of steroid. 5. The possible significance of the results is discussed.

Summary1. The functional integrity of the hypothalamo-pituitary adrenal (HPA) system was assessed in rats after prolonged treatment with tetracosactrin. 2. Adrenal size and sensitivity to corticotrophin were increased. 3. Both the circadian rhythm and the stress-induced increase in HPA activity were inhibited. The circadian rhythm recovered before the response to stress. 4. Tetracosactrin given after betamethasone treatment delayed the return of a normal HPA response to stress. 5. Suppression of HPA activity appeared to be the result of a direct action of tetracosactrin and not entirely due to the elevations in the plasma corticosterone concentration which it caused.

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