The mechanism by which l-NAME-induced hypertension is associated with upregulation of AT1R expression is unknown, but it is possible that NF-κB directly upregulates AT1Rs. In human aortic smooth muscle cells (HASMC) exposed to oxidative stress, AT1R is upregulated in vascular tissue, and this was inhibited by an antioxidant or siRNA against p65 subunit of NF-κB [38]. Here, AGTR1 is linked to hypertensive disorder.