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Effects of angiotensin-converting enzyme gene polymorphism on heart rate and blood pressure variabilities

血管紧张素转换酶基因多态性对心率和血压变异的影响

基本信息

批准号：
08671727
负责人：
KIMURA Tomomasa
金额：
$ 1.47万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1996
资助国家：
日本
起止时间：
1996 至 1998
项目状态：
已结题

项目摘要

The aim of this study was to explore, in patients with complex regional pain syndrome and patients with postherpetic neuralgia, whether this polymorphism (DD and II bomozygotes, and ID heterozygotes) associates heart rate and blood pressure variabilities, and the genetic risk factor for neuropathic pain. The distribution of the DD, ID and II genotypes in the study group is 33%, 33% and 33%, respectively. ACE activity was significantly higher in subjects with the ACE DD genotype than subjects with the ID and II genotypes. No significant difference in heart rate and blood pressure variabilities, plasma renin activity, angiotensin I and II was detected among the ACE genotypes. The frequency of the ACE DD genotype in the present population (33%) was higher than those previously described in other normal populations of the same race (2O%).^3 In addition, the frequency of the ACE DD genotype in CRPS type I was higher than those in CRPS type II.It is possible that the DD genotype favors the development of neuropathic pain as well as cardiovascular disease, perhaps through the presence of higher ACE concentrations. Elevated ACE activity in these subjects may result in increased angiotensin II levels in the effector site, and this might be a mechanism underlying the association between the ACE deletion polymorphism and the increased genetic risk for susceptibility to neuropathic pain. Typing for ACE I/D gene poly-morphism, thus, might be a useful predictor of neuropathic pain.

本研究的目的是探索复杂区域疼痛综合征患者和带状疱疹后神经痛患者中该基因多态(DD和II纯合子，以及ID杂合子)是否与心率和血压变异相关，以及神经病理性疼痛的遗传危险因素。研究组中DD、ID和II型的分布分别为33%、33%和33%。ACE DD基因携带者的ACE活性显著高于ID和II基因携带者。在心率和血压变异性、血浆肾素活性、血管紧张素I和血管紧张素II方面，不同的ACE基因型之间没有显著差异。本组人群中ACE基因DD型频率(33%)高于其他同种族正常人群(2O%)。3此外，CRPS I型患者的DD型频率高于II型患者。提示DD型基因可能有利于神经病理性疼痛和心血管疾病的发生，其机制可能与较高的ACE浓度有关。在这些受试者中，ACE活性升高可能导致效应部位血管紧张素II水平升高，这可能是ACE缺失多态与神经病理性疼痛易感性遗传风险增加之间存在关联的机制之一。因此，ACE I/D基因多态性分型可能是神经病理性疼痛的有用预测指标。