Expression of angiotensin II receptors in aldosterone-producing adenoma of the adrenal gland and their clinical significance

Wu, Zhun; Ni, Dong; Yan, Ye; Li, Jun; Wang, Qianqian; Ouyang, Jinzhi; Zhang, Guoxi; Ma, Xin; Li, Hongzhao; Zhang, Xu

doi:10.1007/s11596-010-0454-0

Cited by 6 publications

(3 citation statements)

References 19 publications

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“…We found that the expression of AT 2 R in APA tissues was lower than that in normal adrenal tissues. But no significant difference in the expression of AT 1 R between adenoma and normal adrenal tissue was revealed [22] . However, the mechanism that underlies the down-regulated AT 2 R remains unclear.…”

Section: Discussionmentioning

confidence: 91%

Association of polymorphisms in angiotensin II receptor genes with aldosterone-producing adenoma

Ouyang

Xing

et al. 2011

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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This study examined the association of polymorphisms in angiotensin II receptor genes (AT (1) R and AT (2) R) with the risk for aldosterone-producing adenoma (APA) in a Chinese Han population. Four polymorphisms including rs5182 (573T/C) in exon 4, rs5186 (1166A/C) in 3'-untranslated region (3'-UTR) in AT (1) R gene and rs5194 (2274G/A) in 3'-UTR, rs1403543 (1675G/A) in intron 1 in AT (2) R gene were detected in 148 APA patients and 192 normal subjects (serving as control) by using a MGB-Taqman probe. The distribution of genotypes of each locus was in accordance with Hardy-Weinberg Equilibrium (HWE) in the APA and control groups (P>0.05). The allele A frequency at rs5194 was significantly higher in the APA group (0.49) than in the control group (0.35) (χ (2)=12.08, P=0.001). Subjects with homozygotic genotype AA and heterozygotic genotype GA were at an increased risk for APA as compared to those with GG genotype (OR=2.66, 95% CI=1.45-4.87; OR=1.67, 95% CI=1.02-2.74). Furthermore, rs5194 single-nucleotide polymorphism (SNP) at AT (2) R gene was significantly associated with APA in additive (OR=1.64, 95% CI=1.21-2.20, P=0.001), dominant (OR=1.94, 95% CI=1.23-3.06, P=0.003), and recessive model (OR=2.01, 95% CI=1.17-3.45, P=0.01). It was concluded that rs5194 polymorphism at AT (2) R gene was associated with the risk for APA, which may constitute a genetic marker of APA.

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Section: Discussionmentioning

confidence: 91%

Association of polymorphisms in angiotensin II receptor genes with aldosterone-producing adenoma

Ouyang

Xing

et al. 2011

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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“…13 Our earlier study preliminarily demonstrated that downregulation of AGTR2, leading to a deficiency in counterbalancing the effects of angiotensin II mediated by AGTR1, could finally promote adrenal zona glomerulosa cell proliferation and aldosterone hypersecretion. 14 According to a series of investigations concerning the connections between AGTR1/2 and the pathology of the adrenal cortex, we speculate that the overexpression of AGTR1 and reduced expression of AGTR2 may be associated with the pathophysiological processes of PA and *The genotypes of additive model were converted to continuous variables to calculate (0="GG"or"CC"; 1="GT"or"CT"; 2="TT"). the relative gene risk variants inevitably involved in this disease, by altering the activity of genes and affecting their transcription and post-transcription.…”

Section: Discussionmentioning

confidence: 99%

Association of polymorphisms in AGTR1 and AGTR2 genes with primary aldosteronism in the Chinese Han population

Huang

Zhou

et al. 2014

J Renin Angiotensin Aldosterone Syst

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Hypothesis: Polymorphisms in angiotensin II type-1/2 receptor genes (AGTR1/AGTR2) may be involved in the pathogenesis of primary aldosteronism. The present study aims to reveal some loci susceptible to the disease on the genes in a group of Chinese Han nationality. Materials and methods: A case-control study was conducted in 202 patients and 188 controls. Ten tagging SNPs on AGTR1/AGTR2 were genotyped for all subjects via the method of multiplex PCR-ligase detection reaction. Statistical analysis was performed with chi-square test and logistic regression analysis. Results: rs3772616 on the AGTR1 gene was a factor for susceptibility to primary aldosteronism (p<0.001), and the TT genotype significantly decreased the risk of primary aldosteronism compared with the CC homozygote (p=0.008, adjusted OR=0.13; 95%CI: 0.03–0.59). The rs3772616 polymorphism was associated with primary aldosteronism under the additive and dominant models. The female carriers of the G allele in rs5193 showed a significant difference compared with the T allele. Conclusions: The AGTR1 rs3772616 polymorphism can be considered as a hereditary marker for primary aldosteronism, and in the Chinese Han population the rs5193 G allele seems to predispose to it only in women.

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“…Aldosterone-producing adenomas express type 1 and type 2 ANG II receptors (AT1R and AT2R respectively) as well as renin, angiotensin, and angiotensinconverting enzyme mRNAs (197,198). However, most of them are unresponsive to the action of ANG II, suggesting the occurrence of post-ANG II receptor defects in aldosterone-producing adenomas.…”

Section: Factorsmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Autocrine/paracrine regulatory mechanisms in adrenocortical neoplasms responsible for primary adrenal hypercorticism

Lefebvre

Prévost

Louiset

2013

European Journal of Endocrinology

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A wide variety of autocrine/paracrine bioactive signals are able to modulate corticosteroid secretion in the human adrenal gland. These regulatory factors, released in the vicinity of adrenocortical cells by diverse cell types comprising chromaffin cells, nerve terminals, cells of the immune system, endothelial cells, and adipocytes, include neuropeptides, biogenic amines, and cytokines. A growing body of evidence now suggests that paracrine mechanisms may also play an important role in the physiopathology of adrenocortical hyperplasias and tumors responsible for primary adrenal steroid excess. These intra-adrenal regulatory systems, although globally involving the same actors as those observed in the normal gland, display alterations at different levels, which reinforce the capacity of paracrine factors to stimulate the activity of adrenocortical cells. The main modifications in the adrenal local control systems reported by now include hyperplasia of cells producing the paracrine factors and abnormal expression of the latter and their receptors. Because steroid-secreting adrenal neoplasms are independent of the classical endocrine regulatory factors angiotensin II and ACTH, which are respectively suppressed by hyperaldosteronism and hypercortisolism, these lesions have long been considered as autonomous tissues. However, the presence of stimulatory substances within the neoplastic tissues suggests that steroid hypersecretion is driven by autocrine/paracrine loops that should be regarded as promising targets for pharmacological treatments of primary adrenal disorders. This new potential therapeutic approach may constitute an alternative to surgical removal of the lesions that is classically recommended in order to cure steroid excess.European Journal of Endocrinology 169 R115-R138

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Expression of angiotensin II receptors in aldosterone-producing adenoma of the adrenal gland and their clinical significance

Cited by 6 publications

References 19 publications

Association of polymorphisms in angiotensin II receptor genes with aldosterone-producing adenoma

Association of polymorphisms in angiotensin II receptor genes with aldosterone-producing adenoma

Association of polymorphisms in AGTR1 and AGTR2 genes with primary aldosteronism in the Chinese Han population

MECHANISMS IN ENDOCRINOLOGY: Autocrine/paracrine regulatory mechanisms in adrenocortical neoplasms responsible for primary adrenal hypercorticism

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