Mechanisms such as normalizing of endothelial NO synthase activity, and reduced cerebrovascular inflammation might also be involved in such protective effects.30 Furthermore, Ang II via AT1 receptors may enhance cerebrovascular permeability and edema by production of ROS and matrix metalloproteinases.31,32 Thus, blocking of AT1 receptors, may reduce ischemic edema by the protective effects on BBB integrity and lowering its permeability during ischemia. Here, AGTR1 is linked to ischemia.