Since we observe that downregulation of Cygb in SMCs and vessels decreases vascular tone and BP with preservation of NO and potentiation of NO signalling, we hypothesized that a decrease in Cygb-mediated NO consumption may be able to compensate for the increase in superoxide-mediated NO consumption that occurs in the vessels of mice with Ang II-induced HTN. Here, AGT is linked to hypertensive disorder.