Importantly, in response to AngII-induced hypertension, such remodelling tends to vary dramatically by region within the murine aorta, with the ascending thoracic aorta susceptible to dilatation, the descending thoracic aorta susceptible to fibrosis, the suprarenal abdominal aorta susceptible to intimo-medial damage and contained rupture and the infrarenal abdominal aorta susceptible to modest remodelling [11]. This evidence concerns the gene AGT and hypertensive disorder.