In addition to the augmented systemic renin-angiotensin system, locally formed Ang II appears to play an important role in the mechanism that affects NO bioavailability, as indicated by the discovery that hypercholesterolemia may trigger the upregulation of vascular chymase, which may be involved in intimal lipid deposition, and may facilitate the development of atherosclerosis [89]. This evidence concerns the gene AGT and atherosclerosis.