Also, in blood vessels chronically exposed to TGF-β1, endothelium-dependent relaxation is lost but can be rescued by inhibiting NADPH oxidase with apocynin or by supplying extra SOD; long-term TGF-β1 overexpression leads to hypertension, cardiac remodeling, and faster atherosclerosis, all of which improve when ROS are blocked or scavenged [101]. This evidence concerns the gene TGFB1 and hypertensive disorder.