Corticotropin-releasing hormone (CRH) directly stimulates corticosterone secretion by the rat adrenal gland.

Corticotropin-releasing hormone (CRH) acute ip administration (10 micrograms) significantly increased the blood concentration of corticosterone (B) in hypophysectomized rats, without inducing any rise in the level of circulating ACTH. CRH (10(-6) M) did not affect B production by isolated rat adrenocortical cells, but notably enhanced that by adrenal slices including both cortex and medulla. This last effect of CRH was blocked by corticotropin inhibiting peptide (CIP), at a concentration (10(-6) M) which was found to completely annul B response of adrenal slices to ACTH (10(-8) M). In light of many findings indicating that adrenal medulla contains and releases CRH and numerous POMC-derived peptides, the hypothesis is advanced that an intra-adrenal CRH/ACTH mechanism may be operative in the control of adrenocortical steroid-hormone secretion.