Role of prostaglandins in adrenal steroidogenesis.
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 potassium-induced 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 less than 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.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000305:Adrenal Cortex Hormones / Q000096:biosynthesis*; D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D011453:Prostaglandins / Q000494:pharmacology / Q000502:physiology*; D051381:Rats
D000305:Adrenal Cortex Hormones; D011453:Prostaglandins; D000804:Angiotensin II; D015121:6-Ketoprostaglandin F1 alpha; D000324:Adrenocorticotropic Hormone; D011188:Potassium; D007213:Indomethacin