Andreis P G, Neri G, Nussdorfer G G
Department of Anatomy, University of Padua, Italy.
Endocrinology. 1991 Feb;128(2):1198-200. doi: 10.1210/endo-128-2-1198.
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.
促肾上腺皮质激素释放激素（CRH）腹腔内急性注射（10微克）可显著提高垂体切除大鼠的皮质酮（B）血浓度，而不会引起循环促肾上腺皮质激素（ACTH）水平升高。CRH（10⁻⁶ M）不影响离体大鼠肾上腺皮质细胞的B分泌，但显著增强了包括皮质和髓质的肾上腺切片的B分泌。CRH的这一最终效应被促肾上腺皮质激素抑制肽（CIP）阻断，发现该浓度（10⁻⁶ M）可完全消除肾上腺切片对ACTH（10⁻⁸ M）的B反应。鉴于许多研究结果表明肾上腺髓质含有并释放CRH和多种源自阿片黑素皮质素原（POMC）的肽，因此提出一种肾上腺内CRH/ACTH机制可能在肾上腺皮质类固醇激素分泌的控制中起作用的假说。
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