Plasma Deoxycorticosterone Levels in Man with Simultaneous Measurement of Aldosterone, Corticosterone, Cortisol and 11-Deoxycortisol

Oddie, C.J.; Coghlan, John P.; Scoggins, Bruce A.

doi:10.1210/jcem-34-6-1039

Cited by 98 publications

(37 citation statements)

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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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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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“…Electrolyte levels were determined with a Technicon auto-analyzer (Technicon Corp., Inc., Tarrytown, NY); cortisol levels were determined by a double isotope derivative dilution assay. 3 Corticotropin was measured by radioimmunoassay (International CIS, Saclay, France).…”

Section: Methodsmentioning

confidence: 99%

Onset and dose relationships of ACTH effects on blood pressure in sheep.

Scoggins¹,

Allen²,

Coghlan³

et al. 1985

Hypertension

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SUMMARY The threshold and dose-response relationships for the blood pressure and metabolic effects of adrenocorticotropic hormone (corticotropin, ACTH) were examined in conscious sheep. Corticotropin was infused at five rates (0.5 jig/kg/day, n -4; 1 /ig/kg/day, n = 4; 2 /xg/kg/day, n = 6; 5 jxg/kg/day, n = 5; and 10 ^tg/kg/day, n = 5) for 3 days, and the time of onset of the rise in blood pressure was assessed with a computer-based system. The effects of equimolar infusion of /3-endorphin and ACTH at 5 ^ig/kg/hour also were examined. Corticotropin infusion at 0.5 ^g/kg/day had no effect on mean arterial pressure. An ACTH infusion of 1.0 /xg/kg/day significantly increased mean arterial pressure (p < 0.001), but the rise was less than that at the three higher doses, all of which produced similar effects. Changes in heart rate were significant at the 10 /xg/kg/day level only (p < 0.01). Initial urinary sodium retention was present at the three higher but not the two lower rates of infusion. Corticotropin infusion had no effect on urinary potassium excretion at any rate but produced hypokalemia at rates of 1.0 /xg/kg/day and above, wTiich appeared to be dose related. Plasma sodium concentration was increased significantly only at the three higher rates (p < 0.001). Urine volume and water intake were increased at ACTH infusion rates of 2.0 to 10 /xg/kg/day. Blood cortisol concentration was increased in the 1 /xg/kg/day group and was maximal in the 2 /xg/kg/day group. Blood corticosterone levels were maximal at infusion rates of 1 /xg/kg/day. A well-defined diurnal rhythm of mean arterial pressure was apparent during the 3 control days. At 10 /xg/kg/day ACTH produced an increase in mean arterial pressure within 8 hours. Infusion of equipotent amounts of ACTH and /3-endorphin did not modify ACTH-induced hypertension. These results indicate that (1) increases in blood pressure can be produced with ACTH infusion at rates that produce plasma ACTH concentrations in the physiological range; (2) the rise in blood pressure occurs within 8 hours of ACTH infusion; (3) ACTH-induced hypertension is unlikely to be due to inhibition of /3-endorphin secretion. (Hypertension 7: 287-291, 1985) KEY WORDS • corticotropin • hypertension • /3-endorphin • corticosteroids T HE administration of adrenocorticotropic hormone (ACTH or corticotropin) to sheep has been shown to produce an adrenally dependent increase in blood pressure within 24 hours, which is associated with hypokalemia and hypernatremia.1 After an initial fall in sodium excretion for 24 to 48 hours, sodium excretion returned to preinfusion values. Urine volume and water intake were increased. In these studies ACTH was injected intramuscularly (Synacthen depot, Ciba-Geigy, Basel, Switzerland) or infused intravenously (Synacthen, Ciba-Geigy) at 20 /xg/kg/day, a rate that has been shown to produce maximal adrenocortical steroid output. 2The aim of the present study was to investigate the threshold and dose-response relationships for the effects of ACTH on blood pressure and ot...

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“…3 mg corticosterone/day in young men (Romanoff & Baxter 1975) or 100-200 mg/day for aldosterone (Katzung 2004, Goodman et al 2007); other authors give higher values for DOC, e.g. (Harris et al 1967), and its plasma concentration is typically 200-400 pmol/l (Brown & Strott 1971, Oddie et al 1972, Schoneshofer et al 1975. Its secretion may be enhanced by ACTH and by angiotensin II and potassium ions, suggesting both a zona fasciculata and a zona glomerulosa origin (Brown et al 1972b), and it is also inevitably enhanced in conditions in which 11b-hydroxylase (CYP11B1) has reduced activity.…”

Section: Effects Of Doc In Manmentioning

confidence: 99%

The mislabelling of deoxycorticosterone: making sense of corticosteroid structure and function

Vinson¹

2011

Journal of Endocrinology

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Over the 70 or so years since their discovery, there has been continuous interest and activity in the field of corticosteroid functions. However, despite major advances in the characterisation of receptors and coregulators, in some ways we still lack clear insight into the mechanism of receptor activation, and, in particular, the relationship between steroid hormone structure and function remains obscure. Thus, why should deoxycorticosterone (DOC) reportedly be a weak mineralocorticoid, while the addition of an 11b-hydroxyl group produces glucocorticoid activity, yet further hydroxylation at C18 leads to the most potent mineralocorticoid, aldosterone? This review aims to show that the field has been confused by the misreading of the earlier literature and that DOC, far from being relatively inactive, in fact has a wide range of activities not shared by the other corticoids. In contrast to the accepted view, the presence of an 11b-hydroxyl group yields, in corticosterone or cortisol, hormones with more limited functions, and also more readily regulated, by 11b-hydroxysteroid dehydrogenase. This interpretation leads to a more systematic understanding of structure-function relationships in the corticosteroids and may assist more rational drug design.

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Plasma Deoxycorticosterone Levels in Man with Simultaneous Measurement of Aldosterone, Corticosterone, Cortisol and 11-Deoxycortisol

Cited by 98 publications

References 1 publication

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

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

Onset and dose relationships of ACTH effects on blood pressure in sheep.

The mislabelling of deoxycorticosterone: making sense of corticosteroid structure and function

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