Lymphocyte-derived adrenocorticotropin is insufficient to stimulate adrenal steroidogenesis in hypophysectomized rats

• Published in: Endocrinology (Philadelphia) Vol. 130; no. 4; p. 2113
• Main Authors: Olsen, N J, Nicholson, W E, DeBold, C R, Orth, D N
• Format: Journal Article
• Language: English
• Published: United States 01-04-1992
• Subjects: Adrenal Cortex Hormones - biosynthesis; Adrenal Glands - metabolism; Adrenocorticotropic Hormone - physiology; Animals; Cell Line; Corticosterone - biosynthesis; Humans; Hypophysectomy; Hypothalamo-Hypophyseal System - physiology; Lymphocytes - physiology; Newcastle disease virus - physiology; Pituitary-Adrenal System - physiology; Pro-Opiomelanocortin - genetics; Rats; RNA, Messenger - analysis
• ISSN: 0013-7227
• DOI: 10.1210/en.130.4.2113

Cells of the immune system can produce and respond to peptide hormones associated with the endocrine system. However, the physiological significance of these endocrine-immune interactions is not known. It has been postulated that cells of the immune system, when stimulated with viruses that induce interferon-alpha, produce sufficient levels of ACTH to stimulate adrenal steroidogenesis and, thus, function as an auxiliary source of ACTH that may have a role in the response to stress. However, we have confirmed that levels of ACTH-related peptides produced by immunocompetent cells are far lower than those produced by the pituitary, raising questions about the ability of lymphocyte-derived ACTH to stimulate adrenal function. Furthermore, we have rigorously examined this issue using intact and hypophysectomized rats treated with Newcastle disease virus. Although high levels of interferon-alpha were produced by both intact and hypophysectomized rats, and the plasma corticosterone concentration increased dramatically in intact animals, corticosterone remained undetectable in hypophysectomized rats. The lack of a corticosterone response in these animals was not due to adrenal insensitivity to ACTH, as shown by a normal rise in corticosterone following Cosyntropin injection 8 h after hypophysectomy. The findings demonstrate that levels of ACTH produced by nonpituitary sources in response to viral infection are not sufficient to stimulate adrenal steroidogenesis.