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Endocrinology, Vol 127, 1904-1909, Copyright © 1990 by Endocrine Society
ARTICLES |
JS Winter, KW Gow, YS Perry and AH Greenberg
Department of Pediatrics, University of Manitoba, Winnipeg, Canada.
Studies using cultured bovine adrenocortical cells now demonstrate that the cytokines interleukin-1 (IL-1) alpha and beta, contrary to previous reports, can stimulate cortisol secretion in vitro in a dose- and time- dependent fashion. However detectable levels of IL-1 receptor could not be demonstrated in adrenal cortical, medullary, or capsular cells by membrane displacement of iodinated IL-1 alpha by unlabeled IL-1 beta, a technique that readily demonstrates specific IL-1 alpha-binding sites on 3T3 fibroblasts. The stimulatory effect of IL-1 on cortisol secretion could be totally blocked by indomethacin, an indication that this effect might be mediated indirectly via local release of prostaglandins (PGs). Subsequent investigations have confirmed that IL- 1 does enhance the conversion of [3H]arachidonate to PGs by cultured adrenal cells, and that some of these PGs (PGD2, PGF2 alpha, and PGE2), in turn, can stimulate cortisol production. Taken together these observations suggest that IL-1-induced stimulation of cortisol secretion is mediated through local release of PGs by a small subpopulation of cells within the adrenal gland.
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