Angiotensin II and glucocorticoid release: direct effect at the adrenal level and modulation of the adrenocorticotropin-induced glucocorticoid release.

Angiotensin II (A II) stimulates adrenal glomerulosa cells releasing mineralocorticoids; however, little is known about the A II effect on glucocorticoids output. The present study has been designed in order to see if A II could modify in vitro spontaneous and ACTH-induced corticosterone (B) release from both fasciculata-reticularis enriched and total adrenal cells. The results indicate that A II at 10(-12), 10(-11), 10(-10) and 10(-6) M concentrations did not modify basal B production and A II 10(-9), 10(-8) and 10(-7) M decreased basal B production from total adrenal cells. Whereas A II (10(-10)-10(-6) M) stimulated B release from fasciculata-reticularis enriched cells. On the one hand, 10(-8) M A II significantly decreased ACTH-elicited B release from total adrenal cells; effect completely abolished by saralasin (SAR, 10(-8) M), a specific A II receptor blocker. On the other hand, 10(-8) M A II did not modify ACTH-induced B release from fasciculata-reticularis enriched cells. Finally, 10(-10) to 10(-6) M A II and 22 pM ACTH stimulated aldosterone output from total adrenal cells; while, fasciculata-reticularis enriched cells did not secrete any measurable amount of aldosterone under basal condition and after incubation with A II. These data further suggest a regulatory role of A II in the release of glucocorticoids from the adrenal gland.