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AJP - Endocrinology and Metabolism, Vol 266, Issue 1 E107-E117, Copyright © 1994 by American Physiological Society
ARTICLES |
L. J. Rosolowsky and W. B. Campbell
Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas 75235-9041.
Intra-adrenal factors promote basal as well as adrenocorticotropic hormone (ACTH)-, angiotensin-, and flow-induced steroid secretion. Because endothelial cells respond to changes in flow and are in a close anatomical relationship to steroidogenic cells, we examined the effect of endothelial cells on the secretion of aldosterone from zona glomerulosa (ZG) cells. Endothelial cells and endothelial cell-conditioned medium (EC-CM) stimulated the release of aldosterone from ZG cells. The stimulatory effect was related to the concentration of endothelial cells or EC-CM. The maximal stimulatory effect was 60-70% of the maximal effect of ACTH. Endothelial cells alone did not produce aldosterone. Human fibroblasts were ineffective in promoting aldosterone release. Endothelial cells and EC-CM failed to stimulate cortisol release from zona fasciculata cells. Treatment of the EC-CM with trypsin and pronase abolished the activity, indicating that a protein mediated the effect. However, the EC-CM activity could be distinguished from angiotensin, endothelin-1, and bradykinin. The factor stimulated the formation of pregnenolone but not the conversion of corticosterone to aldosterone. This endothelium-derived steroidogenic factor appeared to be a novel stimulus to aldosterone secretion. This study represents the first demonstration that endothelial cells alter endocrine function in vitro.
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