AGTR1 and endothelial dysfunction: On binding to AngII, also mean to activate the classical arm (ACE/AngII/AT1R), AT1R stimulates vasoconstriction, sodium retention, sympathetic nervous activation, and reactive oxygen species (ROS) generation, coupled with deleterious effects, including endothelial dysfunction and induction of inflammatory, thrombotic, proliferative, and fibrotic processes [14,19,21].