Although we did not examine the role of oxidative stress in the development of hypertension in present study, we would speculate that both Nox1- and Nox2-derived superoxide contribute to independent phases of the hypertension produced in response to Ang II and are mediated via combined and/or temporal activation of vascular, central, as well as renal AT1 receptors (Zimmerman et al., 2002; Ryan et al., 2004; Crowley et al., 2005, 2006). Here, NOX1 is linked to Hypertension.