Persistent elevation of Ang II also triggers an inflammatory response, characterized by the infiltration of macrophages (ED-1), tubular overexpression of macrophage chemotactic and adhesion molecules, such as osteopontin (OPN), MCP-1 and the expression of inflammatory cytokines, ultimately aggravating renal damage induced by hypertension [3,31,32]. This evidence concerns the gene EDA and hypertensive disorder.