The overactivation of RAS in hypertension is associated with the excessive generation of arachidonic acid-derived 20-hydroxyeicosatetraenoic acid (20-HETE), a strong vasoconstrictor, which potentiates systemic vascular bed responses to angiotensin II (Ang II), and additionally impairs endothelial function [8,9]. Here, AGT is linked to hypertensive disorder.