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Endocrinology, doi:10.1210/endo-113-3-992
Endocrinology Vol. 113, No. 3 992-996
Copyright © 1983 by the Endocrine Society.
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Role of Prostaglandins in Adrenal Steroidogenesis*

STEPHEN L. SWARTZ, GORDON H. WILLIAMS and ROBERT R. BUTTERS, JR., THE TECHNICALASSISTANCE

Endocrine-Hypertension Unit, Brigham and Women’s Hospital and Department of Medicine, Harvard Medical School Boston, Massachusetts 02115

Address requests for reprints to: Dr. Stephen L. Swartz, Brigham and Women’s Hospital, 75 Francis Street, Boston, Massachusetts 02115.

Abstract

Using an in vitro rat glomerulosa and fasciculata cell preparation, we studied the role of porstaglandins (PGs) as potential mediators of angiotensin II-, ACTH-, and potassiuminduced adrenal steroidogenesis. The glomerulosa cells primarily produced prostacyclin under basal and stimulated conditions, whereas the fasciculata cells primarily produce PGF2{alpha} Using 6- keto-PGF1{alpha} (the stable hydrolysis product of prostacyclin) and PGF2{alpha} as indices of PG production in glomerulosa and fasciculata cells, respectively, we noted no significant changes in PGs during angiotensin II-, ACTH-, or potassium-induced steroidogenesis. Pretreatment with indomethacin significantly (P < 0.01) inhibited PG production, but did not alter adrenal steroidogenesis. Furthermore, the administration of exogenous PGs did not affect steroidogenesis. We conclude that PGs do not mediate steroidogenesis from rat glomerulosa or fasciculata cells. (Endocrinology 113: 992,1983)

Footnotes

* This work was supported by NIH Grants RR-00888 and 5-ROl- HL-16821 and a grant from the William Randolph Hearst Foundation (Harvard Medical School, no. 60-096-1500-2).

Received November 18, 1982.




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[Abstract] [Full Text] [PDF]




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Copyright © 1983 by The Endocrine Society