Effects of Glucocorticoid Administration on Aldosterone Excretion and Plasma Renin in Normal Subjects, in Essential Hypertension and in Primary Aldosteronism
The raised aldosterone excretion occurring in salt depleted normal subjects and in patients with primary aldosteronism was significantly suppressed by hydrocortisone administration. During sodium depletion, a lesser fall in aldosterone excretion was also produced by dexamethasone in all normal subjects and some of the patients with essential hypertension. Glucocorticoids sometimes produced a slight depression of plasma renin activity both in normal subjects and in patients with essential hypertension. These slight and inconsistent effects on plasma renin level were not thought to be the major cause of the observed suppression of aldosterone. Differences in mineralocorticoid activity, though not apparent from external balances, might explain the more consistent suppression of aldosterone produced by hydrocortisone as compared with dexamethasone. Other possible reasons for the glucocorticoid-induced decreases in aldosterone excretion were considered; it was concluded that neither ACTH suppression nor changes in potassium balance were responsible. A direct inhibitory effect of the glucocorticoid on adrenal aldosterone production would best explain these observations, as well as the suppression of aldosterone secretion produced with sustained administration of corticotropin. Suppression of aldosterone by glucocorticoid in suspected cases of primary aldosteronism should be interpreted with caution, as this finding certainly does not exclude the presence of an aldosteronesecreting adenoma. The autonomy of such adenomas may be questioned in view of the way their activity can be modified by exposure to glucocorticoid.