Apparently Isolated Excess Deoxycorticosterone in Hypertension

Brown, J. J.; Fraser, Robert; Love, David R.; Ferriss, J. B.; Lever, A. F.; Robertson, James I.; Wilson, Ana Maria Miranda Martins

doi:10.1016/s0140-6736(72)91685-6

Cited by 83 publications

(21 citation statements)

References 35 publications

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“…Tetrahydro-DOC (TH-DOC) excretion was elevated in this study, and this is consistent with previous reports that DOC is increased in some 10 " but not all 13 ' ' 4 low-renin hypertensives. DOC, unlike 19-nor-DOC, is a relatively weak mineralocorticoid and is seldom elevated to biologically significant levels.…”

Section: Discussionsupporting

confidence: 93%

Relationship of 19-nor-deoxycorticosterone to other mineralocorticoids in low-renin hypertension.

Griffing¹,

Dale²,

Holbrook³

et al. 1983

Hypertension

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SUMMARY A number of mineralocorticoids have been proposed as etiologic factors in low-renin hypertension. In this study, urinary free 19-nor-deoxycorticosterone (UF 19-nor-DOC) was compared to other mineralocorticoids -aldosterone, deoxycorticosterone (DOC), and 18-OH-DOC, in 11 lowrenin hypertensive patients on a controlled diet in a metabolic unit. Results demonstrated that both UF 19-nor-DOC and tetrahydro-DOC (TH-DOC) excretion were elevated (2086 ± 926, nl = 339-579 ng/day, and 18 ± 7, nl = 5-15 meg/day, respectively), and positively correlated (r = 0.95). Neither 18-OH-DOC nor aldosterone secretion rates were elevated, and neither of these hormones correlated with UF 19-nor-DOC, with exception of the supine plasma aldosterone (SPA) (r = 0.86). In conclusion, both UF 19-nor-DOC and TH-DOC were increased and positively correlated in the present series of hypertensives. This association is possibly indicative of a precursor-product relationship between DOC and 19-nor-DOC. 19-Nor-DOC, furthermore, correlated with supine plasma aldosterone (SPA), which could, in part, reflect their shared adrenocorticotropic hormone (ACTH) dependence.

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Section: Discussionsupporting

confidence: 93%

Relationship of 19-nor-deoxycorticosterone to other mineralocorticoids in low-renin hypertension.

Griffing¹,

Dale²,

Holbrook³

et al. 1983

Hypertension

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show abstract

“…The finding of elevated plasma levels of deoxycorticosterone here in a subject with essential hypertension, and in cases of low renin hypertension (Brown, Ferriss, Fraser, Lever, Love, Robertson, and Wilson, 1972b), as well as in hyperaldosteronism (Biglieri, Slaton, Schambelan, and Kronfield, 1968), remains to be fully explained. However, this high level of mineralocorticoid cannot account for the false positive result in essential hypertension when the rectal pd is used as a screening test for excess aldosterone.…”

Section: Discussionmentioning

confidence: 82%

Rectal potential difference in the diagnosis of aldosterone excess.

Beevers¹,

Morton²,

Tree³

et al. 1975

Gut

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SUMMARY Rectal potential difference (pd) is directly related to the plasma aldosterone concentration, and rises when aldosterone is stimulated by sodium deprivation. However, when the measurement of rectal pd was tested at a screening test for hyperaldosteronism in 19 hypertensive subjects, four of the eight with primary hyperaldosteronism had a normal pd and four of the eight without aldosterone excess had an abnormally raised potential difference. The technique cannot therefore be recommended as a routine screening test for hyperaldosteronism. No relationship was found between rectal pd and hypertension associated with excess of deoxycorticosterone. Rectal pd rises in response to the mineralocorticoid-like agent carbenoxolone.

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“…Of particular interest in this regard is deoxycorticosterone. In normals, the plasma deoxycorticosterone concentration is around 7-10 ng/dl or 0.2-0.3 nM (17,41,42). Concentrations of this steroid in the 20-100 ng/dl range have been reported in low-renin essential hypertension (17).…”

Section: Discussionmentioning

confidence: 99%

Aldosterone receptors and the evaluation of plasma mineralocorticoid activity in normal and hypertensive states.

Baxter¹,

Schambelan²,

Matulich³

et al. 1976

J. Clin. Invest.

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A B S T R A C T 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-deoxycorticosterone and 18-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 18-hydroxydeoxycorticosterone contribute little to receptor occupancy. Two steroids implicated in low-renin essential hypertension, 16i#-hydroxy-dehydroepiandrosterone 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 samThis work has been published in abstract form: 1975.

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Apparently Isolated Excess Deoxycorticosterone in Hypertension

Cited by 83 publications

References 35 publications

Relationship of 19-nor-deoxycorticosterone to other mineralocorticoids in low-renin hypertension.

Relationship of 19-nor-deoxycorticosterone to other mineralocorticoids in low-renin hypertension.

Rectal potential difference in the diagnosis of aldosterone excess.

Aldosterone receptors and the evaluation of plasma mineralocorticoid activity in normal and hypertensive states.

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