Simultaneous Measurement of Secretory Rates of Aldosterone and 18-Hydroxycorticosterone

Ulick, Stanley; Vetter, K

doi:10.1210/jcem-25-8-1015

Cited by 59 publications

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“…La secretion d'aldosterone est inferieure a 5 ftg/24 h au cours de l'epreuve de restriction sodee, contrastant avec un taux de secretion de corticosterone atteignant 8600 ,ag/24 h. Une nouvelle epreuve de stimulation par PACTHretard fait monter les 17-hydroxycorticosteroides urinaires a 3,4 mg/24 h. [20]. L'activiterenineplasmatique est de 88,8 ng/l/min.…”

Section: Resultats Caslunclassified

“…L'augmentation de la secretion de corticosterone est due au blocage enzymatique et a Paugmentation de la renine. En effet, si la plus grande partie de la corticosterone est sous la dependance de PACTH [20], une fraction est elaboree sous Pinfluence de Pangiotensine comme cela a pu etre demontre au cours d'epreuves de restriction sodee et en presence de dexamethasone chez des sujets recevant un inhibiteur de la synthese d'aldosterone [1]. Par contre chez le sujet normal la seule restriction sodee, malgre Paugmentation de Pangiotensine plasmatique, ne determine pas de variation significative de la secretion de corticostirone [13].…”

Section: Discussionunclassified

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Hypoaldostéronisme congénital familial par défaut de la 18-OH-déhydrogénase: Etude hormonale avant et après guérison du syndrome de perte de sel

et al. 1968

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ExtractIn one case studied from the neonatal period through a follow-up period at almost five years of age, a salt-losing syndrome could be related to a defect in 18-OH-dehydrogenase.In the intial course of the disease, treatment with desoxycorticosterone acetate controlled the saltlosing tendency. At that time, the rate of aldosterone secretion was less than 10 ,ag/day and that of urinary tetrahydroaldosterone was less than S^g/day. In contrast, the rate of corticosterone secretion was 5400 / «g/day and the F:B ratio was 0.8. Urinary 18 hydroxytetrahydro A (18 OH-THA) was increased to 128^g/24 h. There was no cortisol insufficiency; secretion rate was 20 mg m 2 /day and plasma ACTH 0.24 mU/100 ml plasma. At 20 months of age, treatment was stopped because of hypernatremia. From that time on, the child was clinically normal and received no salt supplement.The hormonal results were as follows: At 22 months of age, the secretion rate of aldosterone was less than 5 /tg/day and of corticosterone was 8600 / «g/day on the sixth day of a well-tolerated salt suppression test. 18 OH-THA was 116,ag/day; the F:B ratio for urinary metabolites was low, 0.9.At 3 years and 7 months of age, excretion of urinary tetrahydroaldosterone was 10 ^g/day, 18 OH-THA was in the normal range, and the F:B ratio remained low, 0.6 (normal salt intake).At 4 years and six months of age, secretion rate was 19 ,wg/day and the 18 hydrocorticosterone secretion rate was 470 ,«g/day (ratio 18 OH-B: aldosterone 24.7). Plasma renin activity was 88.8 ng/l/min.The brother of the propositus was observed when 6 years of age. Urinary tetrahydrosterone was 27 ,«g/day, 18 OH-THA was 75 / Mg/day, and the urinary F:B ratio was 0.7 while receiving a normal salt intake.The spontaneous clinical improvement of subjects with the salt-losing syndrome is possibly related to the appearance of a certain amount of aldosterone, an increase in secretion of corticosterone, and modification in salt content of a normal diet during this period. SpeculationA salt-losing syndrome due to 18-OH-dehydrogenase deficiency, probably familial, improved spontaneously. Long-term studies showed persistence of the biosynthetic defect. The data presented raise questions concerning clinical recovery that could be correlated with steroid administration and, possibly, with modifications in sodium homeostasis at that period of life.

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Section: Discussionunclassified

Hypoaldostéronisme congénital familial par défaut de la 18-OH-déhydrogénase: Etude hormonale avant et après guérison du syndrome de perte de sel

et al. 1968

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“…The eluate was dissolved in methylene chloride, washed 1 The chromatographic mobilities of frog tetrahydroaldosterone differed slightly from those of the major-metabolite in human urine, the 3a-hydroxy-5,8 isomer (10). with water, dried and evaporated, and acetylated with acetic anhydride-"C (0.8 mc/mmole) :toluene (1: 4) in pyridine at 60'C for 18 hr and excess reagents removed by partition (11). The triacetate was chromatographed on the Bush A and methylcyclohexane-formamide systems in which it migrated at approximately 1.1 times the rate of deoxycorticosterone acetate.…”

Section: Methodsmentioning

confidence: 99%

Metabolism and rate of secretion of aldosterone in the bullfrog

Ulick¹,

Feinholtz²

1968

J. Clin. Invest.

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A study of the metabolism of aldosterone in the bullfrog was undertaken to provide a measurable metabolite for the indirect isotope dilution technique for measuring secretory rates. The rate of excretion of labeled aldosterone was considerably slower in the frog than in man and made necessary the collection of excretory products for 5 days to insure reasonably complete recovery of metabolites. The major identifiable metabolite was a tetrahydro derivative subsequently identified as 3,f-hydroxy-5,8-tetrahydroaldosterone. This metabolite was excreted partly in the free form and partly as a glucuronic acid conjugate. The pH 1-hydrolyzable conjugate of aldosterone was not detected.For the measurement of secretory rates, aldosterone-3H was injected into the dorsal lymph space and the animal placed in a bath to provide an environment of constant electrolyte composition and intake and a means of collecting excretory products. Urine and bath fluid were collected for 5 days, tetrahydroaldosterone was isolated, and its specific activity determined for the calculation of the aldosterone secretory rate. The rate of secretion of aldosterone in the bullfrog was increased by a tap water bath and by bovine adrenocorticotropic hormone, decreased by a saline bath and by dexamethasone, and unchanged by valine-5-angiotensin amide.

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“…After oxidation of aldosterone and 18-hydroxycorticosterone to their corresponding etiolactones, as described by Ulick and Vetter (14), the procedure of Tait, Tait, Okamoto, and Flood (15) was then used for purification and quantitation of the etiolactones of aldosterone and 18-hydroxycorticosterone by extraction with methylene chloride, washing with sodium bicarbonate and development in a Bush-type paper chromatographic system, cyclohexane: benzene: methanol: water (5: 3:5:1). The paper was then sprayed with blue tetrazolium solution in sodium hydroxide and heated gently for development of soda fluorescence.…”

Section: Isolation and Quantitation Of Aldosterone And 18-hydroxycortmentioning

confidence: 99%

“…in view of this, the differential effect of angiotensin infusion on 24-hr aldosterone secretory rate in the patients with primary and secondary aldosteronism might be explained on the basis of differences in the activity of the renin-angiotensin system at the time of the infu- (14,16). For any single adrenal, the production of 18-hydroxycorticosterone always exceeded that of aldosterone.…”

Section: Isolation and Quantitation Of Aldosterone And 18-hydroxycortmentioning

confidence: 99%

Activation of aldosterone secretion in primary aldosteronism

Spark¹,

Dale²,

Kahn³

et al. 1969

J. Clin. Invest.

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A B S T R A C T Angiotensin infusion evokes marked increases in aldosterone secretion in primary aldosteronism and little change in secondary aldosteronism. The low plasma renin activity of primary aldosteronism and the elevated plasma renin activity of secondary aldosteronism are thought to account for this differential response. The effect of angiotensin on aldosterone and 18-hydroxycorticosterone secretion was studied during adrenal vein catheterization in seven patients with primary aldosteronism (whose plasma renin activity had been elevated following spironolactone therapy), one hypertensive patient with normal plasma renin activity and normal aldosterone secretion, two patients with secondary aldosteronism who had elevated plasma renin activity, and one anephric patient whose plasma renin activity was 0. Adrenal venous aldosterone and 18-hydroxycorticosterone were measured before and after a ten min sub-pressor angiotensin infusion.

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Simultaneous Measurement of Secretory Rates of Aldosterone and 18-Hydroxycorticosterone

Cited by 59 publications

References 0 publications

Hypoaldostéronisme congénital familial par défaut de la 18-OH-déhydrogénase: Etude hormonale avant et après guérison du syndrome de perte de sel

Hypoaldostéronisme congénital familial par défaut de la 18-OH-déhydrogénase: Etude hormonale avant et après guérison du syndrome de perte de sel

Metabolism and rate of secretion of aldosterone in the bullfrog

Activation of aldosterone secretion in primary aldosteronism

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