Aldosterone receptors from rat kidney slices were utilized in a competitive binding technique to analyze the contribution of various
steroids to plasma "
mineralocorticoid" activity and to assess their possible role in
hypertension. To consider simultaneously the plasma binding,
steroids were incubated with slices in undiluted plasma; competitor activities for [3H]
aldosterone binding were
aldosterone, 100%;
deoxycorticosterone, 16.2%;
cortisol, 0.4%; and 18-hydroxy-deoxy-corticosterone and d18-hydroxy-corticosterone, 0.1%. These
steroids were more active in
buffer than plasma, suggesting that they bind to plasma and that this reduces their receptor binding. Analysis of the competition data suggests that at normal plasma concentrations,
aldosterone occupies the receptors to a major extent,
cortisol occupies some of the receptors, and
deoxycorticosterone and 8-hydroxydeoxycorticosterone contribute little to receptor occupancy. Two
steroids implicated in low-
renin essential hypertension, 16beta-hydroxy-dehydro-epiandrosterone and
16-oxoandrostenediol, did not have significant competitor activity. Competitor activity in plasmas from normal subjects taken at 12 noon (upright) was greater than that in those taken at 8 a.m. (supine). Since the 12 noon samples had higher
aldosterone and lower
cortisol levels than the 8 a.m. samples, the competitor activity under these physiological circumstances reflects
aldosterone more than
cortisol. The competitor activities of plasmas from patients relative to normal subjects (100+/-12.1%; mean+/-SEM) were: normal
renin "
essential" hypertension, 117+/-14%; low-
renin essential hypertension, 101+/-6.6%; and primary
aldosteronism, 176+/-14.3%. Thus a significant increase in activity of
steroids that interact with
mineralocorticoid receptors was detected in primary
aldosteronism (P LESS THAN 0.01) BUT WAS NOT DETECTED IN LOW-
RENIN OR NORMAL-
RENIN ESSENTIAL HYPERTENSION.