Interaction of angiotensin I-converting enzyme insertion-deletion polymorphism and daily salt intake influences hypertension in Japanese men

Interaction of angiotensin I-converting enzyme insertion-deletion polymorphism and daily salt intake influences hypertension in Japanese men
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DOI:
10.1291/hypres.29.751
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发表时间:
2006-10-01
影响因子:
5.4
通讯作者:
Muramatsu, Masaaki
Muramatsu, Masaaki
中科院分区:
医学2区
文献类型:
--
作者:
Zhang, Ling;Miyaki, Koichi;Muramatsu, Masaaki

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血管紧张素I转换酶插入缺失多态性(ACE I/D)对盐敏感性高血压的影响已通过盐负荷试验进行了广泛研究,但与每日盐摄入量的相互作用是否影响血压仍有待阐明。因此,我们对 284 名日本男性工人(年龄范围:20-64 岁)进行了一项横断面研究,以检验 ACE I/D 基因型和每日盐摄入量对高血压的影响。测量血压并通过聚合酶链反应 (PCR) 鉴定 ACE I/D。每日盐摄入量是根据食物频率调查问卷(FFQ)计算的。在多变量分析中,我们通过逻辑回归分析和多元线性回归分析探讨了 ACE I/D 与盐摄入量的相互作用。 ACE I/D 本身与血压水平或高血压无关。 ACE I/D 与每日盐摄入量相互作用,并与高血压相关(相互作用 p = 0.047)。在 ID+II 基因型中,高盐摄入会增加高血压(p=0.005),而在 DD 基因型中则不会(p=0.257)。超重组中的相互作用比非超重组中更显着(p=0.039)。在超重组中,高盐摄入导致 ID+II 基因型的舒张压比 DD 基因型高 10.5 mmHg (p=0.042)。我们的结果表明 ACE I/D 和每日盐摄入量构成基因-环境相互作用,可能会受到超重的进一步调节。
The contribution of angiotensin I-converting enzyme insertion-deletion polymorphism (ACE I/D) to salt-sensitivity hypertension has been extensively studied by means of salt-loading tests, but whether or not the interaction with daily salt intake affects blood pressure still remains to be clarified. We therefore conducted a cross-sectional study of 284 Japanese male workers (age range, 20-64 years) to examine the effect of ACE I/D genotype and daily salt intake on hypertension. Blood pressure was measured and the ACE I/D was identified by polymerase chain reaction (PCR). Daily salt intake was calculated from a food frequency questionnaire (FFQ). In multivariate analyses, we explored the interaction of ACE I/D and salt intake by means of logistic regression analysis and multiple linear regression analysis. ACE I/D per se was not associated with blood pressure levels or hypertension. ACE I/D interacted with daily salt intake and correlated with hypertension (p for interaction = 0.047). In the ID+II genotype, hypertension was increased by high salt intake (p=0.005), while in the DD genotype it was not (p=0.257). The interaction was more prominent in the overweight group (p=0.039) than in non-overweight group. In the overweight group, high salt intake induced a 10.5 mmHg higher diastolic blood pressure in the ID+II genotype than in the DD genotype (p=0.042). Our results suggest that ACE I/D and daily salt intake constitute a gene-environment interaction, which may be further modulated by overweight.