Although the mechanism of AngII‐induced endothelial dysfunction remains uncertain, described mechanisms of action include direct binding and inhibition by the AT1 receptor to membrane‐localized eNOS (Marrero et al., 1999), eNOS uncoupling and supervenient superoxide production (Mollnau et al., 2002; Rajagopalan et al., 1996), and upregulation of arginase‐1 leading to reduced substrate availability (Shatanawi et al., 2011). Here, AGTR1 is linked to endothelial dysfunction.