The Effect of Angiotensin II and Saralasin on 18-Hydroxy-ll-Deoxycorticosterone Production by Isolated Human Adrenal Glomerulosa Cells*

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Abstract
To assess the role of angiotensin II (All) in regulating 18-hydroxy-ll-deoxycorticosterone (18-0HD0C) secretion in man, isolated human adrenal glomerulosa cells were incubated with All and/or its competitive antagonist, saralasin. All (2.4 × 108 M) elicited an 80% increase in 18-OHDOC levels as well as similar increases in aldosterone, 18-hydroxycorticosterone, and corticosterone (P < 0.01). Saralasin (108 M) caused a partial but significant inhibition of All-stimulated 18-OHDOC production, while 106 M saralasin blocked All-stimulated steroidogenesis completely. In addition, both concentrations of saralasin caused 10–30% decrements in basal steroid levels. The direct All effect on 18-OHDOC secretion and the antagonistic effect of saralasin on both exogenous and endogenous All-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 bedue to a direct effect on the glomerulosa cell.