The biosynthetic preparation of [16-3H]aldosterone and [16-3H]corticosterone

Ayres, P. J.; Pearlman, William H.; Tait, John; Tait, S. A. S.

doi:10.1042/bj0700230

Cited by 21 publications

(4 citation statements)

References 12 publications

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“…Early reports which showed that aldosterone and 18-hydroxycorticosterone (18-OH-B) are synthesized concomitantly under many conditions suggested that 18-OH-B is an intermediate in the synthesis of aldo¬ sterone, and that the pathway involves the hydroxylation of corticosterone at C-18 followed by dehydrogenation (Ayres, Pearlman, Tait & Tait, 1958;Vecsei, Lommer & Wolff, 1968). Later, this view was refined to suggest that 18-OH-B is converted by a second hydroxylation at C-18, leading to the formation of aldosterone through spontaneous loss of water (Ulick, 1976;Aupetit, Accarie, Emeric et al 1983).…”

Section: Introductionmentioning

confidence: 99%

Origin of aldosterone in trypsin-stimulated rat adrenal zona glomerulosa incubations

Vinson

Laird²,

Hinson³

et al. 1992

Journal of Endocrinology

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The time-course for the in-vitro secretion of aldosterone and 18-hydroxycorticosterone (18-OH-B) by rat adrenal whole capsular tissue (largely zona glomerulosa) was studied under control and stimulated conditions. The stimulatory effect of trypsin was relatively delayed, and the steroids were significantly enhanced only after 1 h, in contrast to the actions of ACTH, which produced effects after 15 or 30 min. Tissue-sequestered 18-hydroxydeoxycorticosterone (t-18-OH-DOC), which is not affected by ACTH, was significantly depleted by trypsin, but secreted 18-OH-DOC was not consistently affected by either stimulant. In contrast to the apparent mobilization of t-18-OH-DOC, the conversion of exogenously added [3H]18-OH-DOC to [3H]18-OH-B was inhibited by trypsin, and aldosterone was unaffected. When trilostane was added to inhibit de-novo steroidogenesis, under conditions in which the steroid secretory response to ACTH is completely inhibited, aldosterone and 18-OH-B secretion was still stimulated by trypsin although yields were lower. Compared with controls, trilostane reduced t-18-OH-DOC concentrations, and trypsin caused a further depletion. In other studies, glomerulosa plasma membrane enriched preparations were homogenized and centrifuged, and the supernatants were dialysed and added to incubations of dispersed zona glomerulosa cells in the presence or absence of stimulators of aldosterone secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Introductionmentioning

confidence: 99%

Origin of aldosterone in trypsin-stimulated rat adrenal zona glomerulosa incubations

Vinson

Laird²,

Hinson³

et al. 1992

Journal of Endocrinology

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“…The steroids were dissolved in a 0-08% solution of beeswax in chloroform and the solution was deposited on a circular planchet that had a series of concentric grooves on its surface. The method is described by Ayres, Pearlman, Tait & Tait (1958). 3-Acetoxyoestra-1,3,5(10),6-tetraen-17-one (1).…”

Section: Methodsmentioning

confidence: 99%

The preparation of [6,7-3H2]oestrogens

O'Donnell¹,

Preedy²,

Pearlman³

1964

Biochemical Journal

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derivative into the same range as those of the 16-deoxy steroids with respect to the 21-alcohol, but the AR,m of the etienic acid with respect to either 21-hydroxy or 21-deoxy derivatives was much more negative than those of the 16-deoxy-17-hydroxy steroids or 16,17-dideoxy steroids. These results confirm that neighbouring groups may have a profound effect on the R , values of reactive groups of steroids. By assuming the validity of Martin's postulates, it should be possible to show that these neighbouring groups affect the mobilities and ARM values in a characteristic and predictable manner. SUMMARY 1. A procedure is described for the characterization of the steroid 17,B-ketol side chain by comparison of the mobilities of the steroid, its 21dehydro and etienic acid derivatives by using thin-layer chromatography.2. A technique for preparing these derivatives on a small scale is described.3. The difference in RM, i.e. AR., between the 21-hydroxy steroids and 21-dehydro steroids was constant for 13 steroids; ARM values for etienic acids were divided into two groups, dependent on the presence or absence of a 17cx-hydroxy group.4. By using the procedure described, steroids that contained the 17-ketol side chain could be readily distinguished from those that did not contain this grouping.

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“…Aldosterone is synthesized in the zona glomerulosa of the adrenal [35] and released upon stimulation by angiotensin II, potassium, and acutely by ACTH and other peptides [36,37]. Aldosterone secretion rates in the human were initially measured by the isotope dilution method using [ 3 H]-aldosterone produced by incubating [ 3 H]-progesterone with adrenal glands, then purified [38]. A known amount and specific activity of [ 3 H]-aldosterone was administered intravenously in humans, then an aldosterone metabolite (tetrahydroaldosterone or aldosterone-18-oxo-glucuronide) was isolated from the urine and its specific activity measured.…”

Section: Metabolism Of Aldosteronementioning

confidence: 99%

An Abbreviated History of Aldosterone Metabolism, Current and Future Challenges

Gómez-Sánchez

2023

Exp Clin Endocrinol Diabetes

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The initial isolation of adrenal steroids from large quantities of animal adrenals resulted in an amorphous fraction resistant to crystallization and identification that had potent effects on electrolyte transport. Aldosterone was eventually isolated and identified in the fraction and was soon shown to cause hypertension when in excess. The autonomous and excessive production of aldosterone, primary aldosteronism, is the most common cause of secondary hypertension. Aldosterone is metabolized in the liver and kidney and its metabolites conjugated with glucuronic acid for excretion. The most common liver metabolite is 3,5-tetrahydroaldosterone-3-glucuronide; that of the kidney is aldosterone-18-oxo-glucuronide. Their values, especially the aldosterone-18-oxo-glucuronide, are commonly used for the diagnosis of primary aldosteronism because they provide and integrated value of the total daily production of aldosterone. Conversion of aldosterone to 18-oxo-glucuronide is impeded by drugs, like some common NSAIDS that compete for UGT2B7, the most important glucuronosyltransferase for aldosterone metabolism. Tetrahydroaldosterone is the most abundant metabolite and most reliable for the diagnosis of primary aldosteronism, but is not commonly measured.

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The biosynthetic preparation of [16-3H]aldosterone and [16-3H]corticosterone

Cited by 21 publications

References 12 publications

Origin of aldosterone in trypsin-stimulated rat adrenal zona glomerulosa incubations

Origin of aldosterone in trypsin-stimulated rat adrenal zona glomerulosa incubations

The preparation of [6,7-3H2]oestrogens

An Abbreviated History of Aldosterone Metabolism, Current and Future Challenges

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