The cause of high blood pressure was a greater peripheral vascular resistance, conditioned by a decrease in the area of glomerular filtration, mesangial proliferation, tubulointerstitial inflammation and glomerulosclerosis (renal remodeling), in addition to the production of ROS stimulated by Ang II at the AT1 receptor upon the activation of Nox. Here, AGTR1 is linked to hypertensive disorder.