Abstract
Suppressed plasma renin activity (PRA) and volume dependent hypertension have been associated with adrenocortical structural abnormalities, excessive deoxycorticosterone, 18-hydroxydeoxycorticosterone (18-OH-DOC) hypersecretion or non-suppressible aldosterone secretion and may be observed in patients thought to have “essential” hypertension. Dale and Melby (1973) encountered an additional alteration in steroid metabolism in two such patients while studying steroidogenesis in vitro by their sectioned adrenals. Conversion of labeled 18-OH-DOC to a new structure 16α,18-dihydroxydeoxycorticosterone was demonstrated to be greatly accelerated by the adrenal tissue in these patients as compared to normal adrenal tissue (70–80% vs 15% conversion). Hypersecretion of 16α,18-dihydroxy-deoxycorticosterone occurred in each. This steroid exerted no effect on sodium metabolism in adrenalectomized rats and in the toad bladder assay, but markedly enhanced activity of subthreshold doses of aldosterone in reducing sodium excretion in urine of adrenalectomized rats. We have concluded that excessive 16α,18-dihydroxydeoxycorticosterone secretion may be important in the genesis of suppressed renin in some patients with hypertension because of the unique activity of this steroid which appears to function as a cooperative or positive allosteric effector of aldosterone.
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