Lower prevalence of the OCT2 Ser270 allele in patients with essential hypertension

Lower prevalence of the OCT2 Ser270 allele in patients with essential hypertension
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DOI:
10.1080/10641960600946411
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发表时间:
2006-10-01
影响因子:
12.3
通讯作者:
Schoemig, Edgar
Schoemig, Edgar
中科院分区:
医学4区
文献类型:
--
作者:
Lazar, Andreas;Zimmermann, Tim;Schoemig, Edgar

文献摘要

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肾脏多巴胺能通路的损伤已被证明会导致原发性高血压。有机阳离子转运蛋白2(OCT2,SLC22A2)与肾脏多巴胺处理以及循环儿茶酚胺的失活有关,并被认为参与血压调节。本研究调查了OCT 2 Ala270Ser多态性与原发性高血压的相关性及其对607例接受左心导管插入术的白人患者血压状态的影响。记录临床特征和诊断,并通过血管内测量确定血压。基因型的比较显示,与野生型等位基因Ala 270的纯合子携带者相比,具有Ser 270等位基因的患者较少受到高血压临床诊断的影响(Kruskal沃利斯检验,p = 0.028)。这种关系在无糖尿病的患者亚组中更为明显(Kruskal沃利斯检验,p = 0.013)。总之,在候选基因分析的背景下提供了关于OCT 2的第一批数据。Ala270Ser多态性与原发性高血压显著相关。这项研究进一步表明了OCT 2在血压稳态中的功能,并指出了转运蛋白在原发性高血压发展中的潜在作用。
Impairment of the renal dopaminergic pathway has been shown to result in essential hypertension. The Organic Cation Transporter 2, OCT2 (SLC22A2), has been implicated in renal dopamine handling as well as in the inactivation of circulating catecholamines and is supposed to be involved in blood pressure regulation. This study investigated the association of the OCT2 Ala270Ser polymorphism with essential hypertension and its impact on blood pressure status in 607 Caucasian patients who underwent left heart catheterization. Clinical characteristics and diagnosis were recorded and blood pressure was determined by intravascular measurement. A comparison of genotypes revealed that patients with the Ser270 allele were less frequently affected by the clinical diagnosis of hypertension than homozygous carriers of the wild type allele Ala270 (Kruskal Wallis test, p = 0.028). This relation was even more pronounced in the subgroup of patients without diabetes mellitus (Kruskal Wallis test, p = 0.013). In summary, the first data on OCT2 are presented in the context of a candidate gene analysis. The Ala270Ser polymorphism was significantly associated with essential hypertension in the present sample. This study further suggests a function of OCT2 in blood pressure homeostasis and points to the potential role of the transporter in the development of essential hypertension.