Other recent studies indicate that ROS production is increased in humans with hypertension and several hypertensive animal models [43, 44], and oxidative stress upregulates vascular and renal AT1R via mechanisms involving NF-κB and chronic AT1R blockade significantly reduces an increase of ROS production [45, 46], suggesting an interaction between AT1R, NF-κB, and oxidative stress in the cardiovascular regulatory centres. Here, NFKB1 is linked to hypertensive disorder.