Mice established high blood pressure and an increase in arterial angiotensin II (Ang-II); significant eNOS-dependent superoxide and peroxynitrite accumulation impairment of acetylcholine; an 8.7-fold increase in eNOS mRNA and protein; and Ang-II inhibition with reduced oxidative stress, normalized blood pressure, and endothelium-dependent relaxation. Here, AGT is linked to hypertensive disorder.