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α(2C) - 缺失322 - 325位点的肾上腺素能受体多态性与高血压患者左心室肥厚的发生

The α(2C)-Del322-325 adrenoceptor polymorphism and the occurrence of left ventricular hypertrophy in hypertensives.

作者信息

Savva Jacqueline, Alfakih Khaled, Galloway Stacey L, Hall Alistair S, West Robert M, Ball Stephen G, Balmforth Anthony J, Maqbool Azhar

机构信息

Division of Cardiovascular and Neuronal Remodelling, Leeds Institute of Genetics, Health and Therapeutics, University of Leeds, Leeds, UK.

出版信息

Blood Press. 2012 Apr;21(2):116-21. doi: 10.3109/08037051.2011.622988. Epub 2011 Nov 1.

DOI:10.3109/08037051.2011.622988
PMID:22040172
Abstract

OBJECTIVES

Sympathetic activation has a role in the development of left ventricular hypertrophy (LVH). The presynaptic α(2C)-adrenoceptor inhibits the release of norepinephrine from sympathetic nerve terminals in the heart. A deletion polymorphism in the α(2C)-adrenoceptor (α(2C)Del322-325) generates a hypofunctional α(2C)-adrenoceptor, which may result in chronic adrenergic signalling. This study aimed to investigate whether the α(2C)Del322-325 polymorphism was associated with an increased prevalence of LVH in patients with systemic hypertension.

METHODS

Left ventricular mass was measured in 205 patients with systemic hypertension and 60 normal volunteers using a 1.5-T Philips MRI system. Genotyping was performed using a restriction fragment length polymorphism assay.

RESULTS

No significant difference was observed between the distribution of the α(2C)Del322-325 genotypes in hypertensive patients with LVH compared with those without LVH. Adjusting for confounding variables the odds ratio (OR) of being ins/del for the α(2C)Del322-325 and having LVH was 0.49 (95% CI 0.14-1.69, p = 0.256).

CONCLUSIONS

These observations suggest that there is little evidence for an association between α(2C)Del322-325 polymorphism and an increased prevalence of LVH in patients with systemic hypertension.

摘要

目的

交感神经激活在左心室肥厚(LVH)的发生发展中起作用。突触前α(2C)-肾上腺素能受体抑制心脏交感神经末梢去甲肾上腺素的释放。α(2C)-肾上腺素能受体的一个缺失多态性(α(2C)Del322 - 325)产生功能减退的α(2C)-肾上腺素能受体,这可能导致慢性肾上腺素能信号传导。本研究旨在调查α(2C)Del322 - 325多态性是否与系统性高血压患者LVH患病率增加相关。

方法

使用1.5-T飞利浦MRI系统测量205例系统性高血压患者和60例正常志愿者的左心室质量。采用限制性片段长度多态性分析进行基因分型。

结果

与无LVH的高血压患者相比,有LVH的高血压患者中α(2C)Del322 - 325基因型的分布无显著差异。校正混杂变量后,α(2C)Del322 - 325为ins/del且患有LVH的优势比(OR)为0.49(95%CI 0.14 - 1.69,p = 0.256)。

结论

这些观察结果表明,几乎没有证据支持α(2C)Del322 - 325多态性与系统性高血压患者LVH患病率增加之间存在关联。

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