The effect of sodium deprivation and of angiotensin II infusion on the peripheral plasma concentrations of 18-hydroxycorticosterone, aldosterone and other corticosteroids in man

Abstract

The effect of angiotensin II infusion on plasma cortisol, 11-deoxycorticosterone, corticosterone, 18-hydroxycorticosterone and aldosterone concentrations was compared in 6 normal subjects before and after different degrees of sodium depletion. Cortisol, 11-deoxycorticosterone and corticosterone levels were unaffected by sodium depletion or by angiotensin II infusion in either replete or deplete states. Plasma 18-hydroxycorticosterone and aldosterone concentrations rose in parallel when sodium replete subjects were infused with angiotensin II. Sodium depletion had a proportionately greater stimulating effect on plasma 18-hydroxycorticosterone than on aldosterone, particularly in the more severely depleted subjects. The rise in plasma aldosterone concentration following angiotensin II infusion was greater in sodium deplete than in sodium replete subjects and this difference increased with the severity of sodium depletion. Basal 18-hydroxycorticosterone concentrations were much higher in the sodium deplete state than when the subjects were replete with sodium, but the subsequent effect of angiotensin II infusion, although further increasing 18-hydroxycorticosterone levels, was less consistent. The effect of angiotensin II was not secondary to a rise in ACTH since, in a seventh subject pretreated with dexamethasone, the response was not abolished It is concluded that one effect of angiotensin II must occur at or before 18-hydroxylation in the biosynthetic pathway. The availability of a larger pool of aldosterone precursor as a result of sodium depletion may be an explanation of the phenomenon of sensitization of aldosterone production to angiotensin II infusion in this condition. The possibility of a second effect of angiotensin II on the conversion of 18-hydroxycorticosterone to aldosterone is also discussed.