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 angiotensinⅡ 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.