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Journal ArticleDOI

Estimation of aldosterone, 11-deoxycorticosterone, 18-hydroxy-11-deoxy-corticosterone, corticosterone, cortisol and 11-deoxycortisol in human plasma by gas-liquid chromatography with electron capture detection.

P. A. Mason, +1 more
- 01 Feb 1975 - 
- Vol. 64, Iss: 2, pp 277-288
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TLDR
When seven normal subjects were treated with dexamethasone concentrations of DOC, cortisol and 11-deoxycortisol fell to below the limit of thenormal range, those of 18-OH-DOC and corticosterone were at the lower end of the normal range while the concentration of aldosterone was not significantly affected.
Abstract
A method for determining the plasma concentrations of six major corticosteroids, aldosterone, 18-hydroxy-11-deoxycorticosterone (18-OH-DOC), corticosterone, deoxycorticosterone (DOC), cortisol and 11-deoxycortisol using gas-liquid chromatography with electron capture detection is described. Esterification of suitable derivatives of these compounds with heptafluorobutyric anhydride (HFB) allowed detection of quantitities of steroid, ranging from 0-3 pg for androstenetrione HFB (from cortisol) to 2-3 pg for corticosterone HFB. No detectable reagent blank was obtained for any compound when water was used instead of plasma and this was also the case when plasma from an adrenalectomized subject was analysed, with the exception of 18-OH-DOC where a reproducible but negligibly small blank occurred. Coefficients of variation for replicate determinations ranged from 8% for corticosterone to 17% for aldosterone. Concentrations in a series of normal human plasma samples were as follows: aldosterone, 4-0- 18-0 ng/100 ml; 18-OH-DOC, 20-16- ng/ml; corticosterone, 0-08 - 0.-80 mug/100 ml; DOC, 2-8 - 16-0 ng/100 ml; cortisol, 2-5 - 10-0 mug/100 ml; and 11-deoxycortisol, 40-0 - 400-0 ng/100 ml. When seven normal subjects were treated with dexamethasone concentrations of DOC, cortisol and 11-deoxycortisol fell to below the limit of the normal range, those of 18-OH-DOC and corticosterone were at the lower end of the normal range while the concentration of aldosterone was not significantly affected.

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Journal ArticleDOI

Simultaneous radioimmunoassay of plasma aldosterone, corticosterone, 11-deoxycorticosterone, progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, cortisol and cortisone.

TL;DR: A method for the simultaneous determination of eight major corticosteroid hormones and precursors in 0.5–2.0 ml of plasma has been developed and is described in detail, revealing sex differences between the adults studied with higher A, B and P levels in females and higher 17-OH-P and E levels in males.
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Clinical, biochemical and pathological features of low-renin (“primary”) hyperaldosteronism

TL;DR: The clinical and biochemical findings in 136 patients with low-renin ("primary") hyperaldosteronism are described and it is concluded that this condition is not a benign form of hypertension.
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The effects of ACTH on steroid metabolomic profiles in human adrenal cells

TL;DR: It is illustrated that adrenal cells respond to ACTH through the secretion of a variety of steroid hormones, thus supporting the role of adrenal Cells as a source of both corticosteroids and androgens.
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Calcium antagonists decrease adrenal and vascular responsiveness to angiotensin II in normal man.

TL;DR: Calcium antagonist nifedipine may lower blood pressure via decreased adrenal responsiveness to angiotensin II as well as by peripheral vasodilatation andTransmembrane movement of calcium is involved in the aldosterone response to angiotsin II in man.
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Familial glucocorticoid deficiency. Studies of diagnosis and pathogenesis.

TL;DR: The clinical and biochemical findings are described in 2 brothers who had intermittent hypoglycaemia generally precipitated by the "stress" of infection and showed a failure of adrenocortical response to ACTH which was progressive in the eldest boy.
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