Idiopathic hyperaldosteronism: analysis of aldosterone synthase gene

Miyamori, Isamu; Inaba, Shin-ichi; Hatakeyama, Hyōe; Taniguchi, Naomi; Takeda, Y.

doi:10.1016/s0753-3322(00)80017-7

Cited by 9 publications

(6 citation statements)

References 12 publications

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“…It inhibited basal CYP11B2 promoter activity as well as activation by angiotensin II [24,25] and the nuclear hormone receptors (NGFIB, NURR1) [26] in transfected human adrenocortical cells. Moreover, studies reported the overexpression of CYP11B2 mRNA in the lymphocytes of patients with IHA when compared to normal controls and APA subjects [27,28]. This overexpression of CYP11B2 appeared to parallel the overproduction of aldosterone in the adrenal glands [28] and reinforces the hypothesis of a possible association of -344C allele with decreased IHA risk, at least partly, due to increased binding of SF-1.…”

Section: Discussionsupporting

confidence: 65%

“…Moreover, studies reported the overexpression of CYP11B2 mRNA in the lymphocytes of patients with IHA when compared to normal controls and APA subjects [27,28]. This overexpression of CYP11B2 appeared to parallel the overproduction of aldosterone in the adrenal glands [28] and reinforces the hypothesis of a possible association of -344C allele with decreased IHA risk, at least partly, due to increased binding of SF-1. Besides, the study by Connell et al found that basal and ACTH-stimulated plasma levels of 11-deoxycortisol, the precursor of cortisol, were higher in subjects carrying -344T allele [29].…”

Section: Discussionsupporting

confidence: 65%

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Association of CYP11B2 polymorphisms with susceptibility to primary aldosteronism: a meta-analysis

et al. 2013

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PRIMARY ALDOSTERONISM (PA) is characterized by overproduction of the mineralocorticoid hormone aldosterone by adrenal glands. According to recent reports, it appears to be the most common cause of secondary persistent hypertension, and may account for about 8~13% of unselected hypertensives [1] and as high as 20% of resistant hypertensives [2,3]. The inappropriately high production of aldosterone causes suppression of plasma renin, sodium retention, hypertension, cardiovascular damage, and potassium excretion [4]. Elevated blood pressure combined with the proinflammatory and profibrotic effects of aldosterone To date, although the genetic basis of familial hyperaldosteronism has been more clearly, the exact pathogenesis of sporadic forms of the disease remains unknown. Among a number of studied susceptibility genes, the aldosterone synthase gene (CYP11B2) is the most commonly studied. The CYP11B2 gene situates on chromosome 8q24.3 and encodes aldosterone synthase, which is the key rate-limiting enzyme for the final stage of aldosterone synthesis pathway and pri- Original

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Section: Discussionsupporting

confidence: 65%

Section: Discussionsupporting

confidence: 65%

Association of CYP11B2 polymorphisms with susceptibility to primary aldosteronism: a meta-analysis

et al. 2013

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“…CYP11B2 is present only in the zona glomerulosa (ZG), where its 11β-hydroxylase, 18-hydroxylase and 18-methyl oxidase activities are required to convert deoxycorticosterone to aldosterone (Ogishima et al, 1991; Curnow et al, 1991; Kawamoto et al, 1992). Although CYP11B2 expression appears to be high in IHA and APA (Takeda et al, 1999; Miyamori et al, 2000; Fallo et al, 2002; Bassett et al, 2005), only descriptive low resolution studies using polyclonal antibodies have been published (Nishimoto et al, 2010; Nanba et al, 2013). …”

Section: Introductionmentioning

confidence: 99%

Adrenal CYP11B1/2 expression in primary aldosteronism: Immunohistochemical analysis using novel monoclonal antibodies

Nakamura

Maekawa

Felizola

et al. 2014

Molecular and Cellular Endocrinology

110

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CYP11B1 and CYP11B2 play pivotal roles in adrenocorticosteroids synthesis. We performed semi-quantitative immunohistochemical analysis of these proteins in adrenals from patients with primary aldosteronism using novel monoclonal antibodies. Clusters of cortical cells positive for CYP11B2 were detected in the zona glomerulosa (ZG) of normal adrenal gland (NA), idiopathic hyperaldosteronism (IHA) and the adjacent adrenal of aldosterone-producing adenoma (APA). In APA, heterogenous immunolocalization of CYP11B2 and diffuse immunoreactivity of CYP11B1 were detected in tumor cells, respectively. The relative immunoreactivity of CYP11B2 in the ZG of adjacent adrenal of APA was significantly lower than that of NA, IHA and APA tumor cells, suggestive of suppressed aldosterone biosynthesis in these cells. These findings did indicate the regulatory mechanisms of aldosterone biosynthesis were different between normal/hyperplastic and neoplastic aldosterone-producing cells in human adrenals. CYP11B2 immunoreactivity in the ZG could also serve as a potential immunohistochemical marker differentiating morphologically hyperplastic ZG of IHA and APA adjacent adrenal.

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“…Increased aldosterone synthase activity was measured in isolated mononuclear leukocytes (MNL) of patients with IHA and was significantly increased when compared with that of patients with APA or to normal controls. This increase correlated with increased CYP11B2 mRNA expression in MNL [Miyamori et al 2000]. However, no mutation was detected in the genomic DNA of these patients, so that overexpression of CYP11B2 was attributed to the presence of regulatory factors.…”

Section: Cypb11b2 In Primary Hyperaldosteronismmentioning

confidence: 89%

Hyperaldosteronism in pregnancy

Escher

2009

Therapeutic Advances in Cardiovascular Disease

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Aldosterone is a key regulator of electrolyte and water homeostasis and plays a central role in blood pressure regulation. Hormonal changes during pregnancy, among them increased progesterone and aldosterone production, lead to the required plasma volume expansion of the maternal body as an accommodation mechanism for fetus growth. This review discusses the regulation of aldosterone production by aldosterone synthase (CYP11B2); the impact on aldosterone secretion due to the presence of a chimeric gene originating from a crossover between CYP11B1 and CYP11B2 in glucocorticoid remediable aldosteronism (GRA) - the inherited form of hypertension; enhanced aldosterone production in aldosterone-producing adenoma (APA); and idiopathic hyperaldosteronism (IHA). Features of hyperaldosteronism are also found in patients with apparent mineralocorticoid excess (AME), in which glucocorticoids exacerbate activation of the mineralocorticoid receptor (MR) because of a defect in the 11beta-hydroxysteroid dehydrogenase type 2 enzyme. Regulation of aldosterone production and tissue-specific activation of the mineralocorticoid receptor are prerequisites for optimal control of body fluids and blood pressure during pregnancy and contribute largely to the wellbeing of the mother-to-be.

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Idiopathic hyperaldosteronism: analysis of aldosterone synthase gene

Cited by 9 publications

References 12 publications

Association of CYP11B2 polymorphisms with susceptibility to primary aldosteronism: a meta-analysis

Association of CYP11B2 polymorphisms with susceptibility to primary aldosteronism: a meta-analysis

Adrenal CYP11B1/2 expression in primary aldosteronism: Immunohistochemical analysis using novel monoclonal antibodies

Hyperaldosteronism in pregnancy

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