Simultaneous determination of plasma 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone, and aldosterone in man.

Ojima, Motoko; Aida, Mitsuyasu; Kambegawa, Akira

doi:10.1620/tjem.124.367

Cited by 11 publications

(6 citation statements)

References 20 publications

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“…Certain authors (Martin et al 1975, Chandler et al 1976Williams et al 1976;Ojima et al 1978) measured individual plasma levels of 18-OH-DOC and 18-OH-B, but few evaluated these two steroids simultaneously in the single extract. The major problems for establishing this procedure may be the following three: effective separation of the steroids, adequate purification, and sufficiently sensitive quantitation.…”

Section: Discussionmentioning

confidence: 99%

Plasma concentrations of 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone simultaneously measured in normal subjects and adrenocortical disorders.

Ojima

Kambegawa²

1980

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 99%

Plasma concentrations of 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone simultaneously measured in normal subjects and adrenocortical disorders.

Ojima

Kambegawa²

1980

Tohoku J. Exp. Med.

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“…Other measurements were (1) BP, which was obtained either by a mercury sphygmomanometer and by a finger photoplethysmographic device capable of providing accurate beat-to-beat systolic and diastolic values, [21][22][23] (2) heart rate, which was monitored beat-to beat by a tachograph triggered by the R wave of an ECG, (3) respiration rate, which was measured by a strain gauge pneumograph positioned at midchest level, (4) left ventricular mass index (left ventricular mass divided by the body surface area), which was obtained by bidimensional echocardiography according to the recommendations of the American Society of Echocardiography, 24,25 (5) body mass index (body weight divided by squared height) and waist and hip circumferences, which were obtained with the patient standing and used to calculate the waist-to-hip ratio, and (6) a variety of measurements from a venous blood sample obtained 30 minutes after vein cannulation with the patient in supine position for several minutes: routine hematologic and blood chemistry (standard methods), plasma glucose and serum insulin (standard methods), homeostatic model assessment (HOMA) index (calculated with the following formula 26 : plasma glucose [mmol/L]×serum insulin [μU/mL]/22.5), plasma leptin (ELISA, DRG Instruments GmbH, Marburg, Germany), plasma norepinephrine and epinephrine (high-performance liquid chromatography), 27 plasma renin activity (radioimmunoassay), 28 as well as plasma aldosterone (radioimmunoassay). 29 Simultaneous MSNA, beat-to-beat heart rate, and beat-to-beat BP recordings also allowed to study the baroreflex. To this aim, phenylephrine was infused in an antecubital vein at the doses of 0.3, 0.6, and 0.9 μg kg −1 min −1 to increase BP, stimulate baroreceptors, and reflexly induce a reduction of MSNA and heart rate.…”

Section: Measurementsmentioning

confidence: 99%

Long-Term Sympathoinhibitory Effects of Surgically Induced Weight Loss in Severe Obese Patients

Seravalle

Colombo

et al. 2014

Hypertension

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L ong-term prospective studies have recently shown that bariatric surgery significantly reduces the risk of death in severely obese patients.1 This has been confirmed by retrospective analyses of a large cohort of obese individuals in whom surgery-related reductions in body weight were associated with a significant reduction in death rate compared with obese individuals followed under dietary and medical treatment. [2][3][4] It is a widespread belief that the protective effect of bariatric surgery in obese patients may perhaps be related to a reduction of body weight per se but that the concomitant improvement of the array of risk factors commonly associated with obesity, for example, alterations in lipid and glucose metabolism, is likely to play a major role. [5][6][7] In this context, however, little attention has to date been given to whether bariatric surgery is also associated with the improvement of another adverse phenomenon of obesity (ie, sympathetic activation). 8,9 The only information available comes from 3 studies that assessed sympathetic tone by making use of spectral analysis of heart rate signal or 24-hour norepinephrine urinary excretion [10][11][12] (ie, approaches that display major intrinsic limitations not allowing to provide any direct insight on the effects of the intervention on central sympathetic outflow, as the microneurographic technique only allows to achieve 13 .) The issue has pathophysiological and clinical relevance because sympathetic activation has been shown to be an adverse prognostic factor in several clinical conditions.14-17 Furthermore, evidence has been obtained that sympathetic overdrive may cause or worsen insulin resistance, 18,19 thus contributing to a common metabolic alteration in obesity.Abstract-Weight loss improves insulin sensitivity and exerts sympathomodulatory effects. No data, however, are available on the effects of the weight loss induced by vertical sleeve gastrectomy on sympathetic neural drive, insulin sensitivity, and their reciprocal cross talks. In 10 severe obese hypertensives (age, 54.0±2.3 years [mean±SEM]), we measured sphygmomanometric blood pressure, heart rate, body mass index, homeostatic model assessment index, plasma leptin, muscle sympathetic nerve traffic (microneurography), and baroreflex sensitivity (vasoactive drug technique). Measurements were performed 2 to 3 days before surgery and repeated 6 and 12 months after the procedure. Ten matched hypertensive obeses not undergoing gastrectomy served as controls. Six months after bariatric surgery, a significant (P<0.05) reduction in body mass index (−9.1±1.4 kg/m 2 ), sphygmomanometric systolic blood pressure (−10.2±4.5 mm Hg), heart rate (−11.0±2.4 bpm), homeostatic model assessment index (−3-3±1.3 AU), plasma leptin (−53.6±8.8 μg/L), and muscle sympathetic nerve traffic (−15.0±3.4 bursts/100 heart beats) was observed. The weight loss, the plasma leptin reduction, and the sympathetic inhibition were maintained after 12 months, whereas homeostatic model assessment index showed a tendency ...

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“…PRA, plasma aldosterone (Dainabot Co., Tokyo), and plasma ACTH (Midorijuji Co., Tokyo) were estimated using commercial RIA kits. For the determinations of plasma 18-OH-B, 18-OH-DOC, and DOC, the plasma samples were extracted with dichloromethane and the extracts were separated by LH-20 column chromatography and the fractions were estimated radioimmunologically (Ojima et al 1978;Ojima and Kambegawa 1980).…”

Section: Methodsmentioning

confidence: 99%

Evidence for endogenous dopaminergic control of mineralocorticoids secretion in normal subjects and in patients with hyperaldosteronism.

Shimizu

Hanew

Sato

et al. 1984

Tohoku J. Exp. Med.

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The role of endogenous dopamine (DA) in the secretion of several mineralocorticoids was studied in six normal subjects, eight patients with primary aldosteronism (PA), two patients with non-familial idiopathic hyperaldosteronism (NF-IHA), and four patients with familial IHA (F-IHA). To these subjects 10 mg metoclopramide (MCP) was administered intravenously, and plasma aldosterone (Aid), 18-OH-corticosterone (18-OH-B), 18-OH-11-deoxycorticosterone (18-OH-DOC), and DOC were measured by RIA. Further, °five normal subjects were studied with MCP test after pretreatment with DA infusion (5pg/kg/min over 90 min). After the administration of MCP, normal subjects showed significant increases in their plasma Ald and 18-OH-B, and slight increases in plasma 18-OH-DOC and DOC. However, no significant changes were observed in plasma ACTH, cortisol, PRA, or serum K, Na or Cl. In patients with PA and NF-IHA, plasma Ald and the three precursors were increased after administration of MCP. Especially, marked increases in plasma 18-OH-DOC were seen in PA patients. In contrast, F-IHA patients showed increases in the above mineralocorticoids except 18-OH-B. Following DA infusion in normal subjects neither basal plasma Ald secretion nor the responsivenesses to MCP were modified. These results suggest that endogenous DA plays an inhibitory role in the terminal stages of mineralocorticoids production in man. However, the degrees of the dopaminergic inhibition may be different in normal subjects and the patients with mineralocorticoids excess, and among the three groups of aldosteronism mentioned above. endogenous dopamine ; primary aldosteronism ; non-familial idiopathic hyperaldosteronism ; familial idiopathic hyperaldosteronism ; metoclopramide It is well known that the renin-angiotensin system, ACTH, sodium, and potassium are physiological regulators of plasma aldosterone secretion. Recently,

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Simultaneous determination of plasma 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone, and aldosterone in man.

Cited by 11 publications

References 20 publications

Plasma concentrations of 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone simultaneously measured in normal subjects and adrenocortical disorders.

Plasma concentrations of 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone simultaneously measured in normal subjects and adrenocortical disorders.

Long-Term Sympathoinhibitory Effects of Surgically Induced Weight Loss in Severe Obese Patients

Evidence for endogenous dopaminergic control of mineralocorticoids secretion in normal subjects and in patients with hyperaldosteronism.

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