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Journal of Clinical Endocrinology & Metabolism, Vol 49, 600-603, Copyright © 1979 by Endocrine Society
ARTICLES |
LM Braley and GH Williams
To assess the role of angiotensin II (AII) in regulating 18-hydroxy-11- deoxycorticosterone (18-OHDOC) secretion in man, isolated human adrenal glomerulosa cells were incubated with AII and/or its competitive antagonist, saralasin. AII 2.4 X 10(-8) M) elicited an 80% increase in 18-OHDOC levels as well as similar increases in aldosterone, 18- hydroxycorticosterone, and corticosterone (P less than 0.01). Saralasin (10(-8) M) caused a partial but significant inhibition of AII- stimulated 18-OHDOC production, while 10(-6) M saralasin blocked AII- stimulated steroidogenesis completely. In addition, both concentrations of saralasin caused 10--30% decrements in basal steroid levels. The direct AII effect on 18-OHDOC secretion and the antagonistic effect of saralasin on both exogenous and endogenous AII-stimulated steroidogenesis, documented in these experiments, indicate that the increase in 18-OHDOC levels after sodium restriction reported in man is probably mediated by the renin-angiotensin system. Furthermore, because high concentrations of saralasin did not increase aldosterone secretion, the partial agonist properties of saralasin in vivo in man may not be due to a direct effect on the glomerulosa cell.
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