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Interleukin-1beta Stimulates Corticotropin-Releasing Hormone (CRH) and Adrenocorticotropin (ACTH) Release by Rat Adrenal Gland in Vitro. 1993

G Mazzocchi, and F G Musajo, and L K Malendowicz, and P G Andreis, and G G Nussdorfer
Department of Anatomy, University of Padua, Via Gabelli 65, I-35121 Padua, Italy; and Department of Histology and Embryology, University of Poznan, Swiecickiego 6, PL-60781 Poznan, Poland.

CRH and ACTH immunoreactivities (ir) were present in rat adrenal glands but not in adrenocortical autotransplants lacking chromaffin cells. Interleukin-1beta (IL-1beta) dose-dependently elicited CRH-ir and ACTH-ir release by decorticated adrenal fragments mainly composed of zona-medullaris tissue; the minimum effective concentration was 10(-10)/10(-8)M, and the maximal one was 10(-6)M. The IL-1beta (10(-6)M)-induced ACTH release by our preparations was completely blocked by alpha-helical-CRH (10(-6)M), a competitive inhibitor of CRH. These findings suggest that chromaffin medullary cells of the rat adrenals contain a CRH/ACTH system, duplicating that operating at the hypothalamohypophyseal level, which is stimulated by IL-1beta. Thus, the mechanism underlying the well-known glucocorticoid secretagogue effect of interleukins may involve the activation of both the central and the peripheral branch of the hypothalamohypophyseal-adrenal axis.

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