中文摘要：

原发性高血压（简称高血压病）是遗传和环境因素相互作用所导致的一种复杂性疾病.近年来的研究发现,高血压病的发生和发展与DNA甲基化密切相关.11β-HSD-2、ECE-1和AT1b等基因发生甲基化和去甲基化会影响代谢酶和受体的表达,从而通过肾素-血管紧张素-醛固酮系统激活以及肾性水钠潴留等途径引起高血压的发生,这可能是高血压发病的一个重要分子机制.基因组低甲基化（如：高同型半胱氨酸所引起的）会诱发AT1b、ECE-1等受体和代谢酶基因发生去甲基化,从而参与高血压病的发生.深入了解DNA甲基化调控在原发性高血压发病过程中的分子机制及药物代谢酶和受体基因甲基化状态的改变对高血压患者降压疗效的影响,将为临床制定合理化的用药方案提供依据.

英文摘要：

Essential hypertension （EH） is a complex disease caused by interaction of genetic and environmental factors. Increasing evidences suggest that hypomethylation of certain genes is involved in pathogenesis of EH. Alteration in methylation status affects expression of genes encoding 11β-hydroxysteroid dehydrogenase-2 （11β-HSD-2）, endothelin converting enzyme-1 （ECE-1） and angiotensin Ⅱ receptor type 1b （AT1b） and hence results in hyperactivation of renin-angiotensin-aldosterone system and reduced renal sodium retention. Genomic hypomethylation can be induced by homocystine （Hcy）. Study of metabolizing enzyme and receptor gene methylation regulation and its relation to antihypertensive effects will help understand the pathogenesis of EH and provide evidence for improving clinical treatment of EH.