Besides that, non-catecholaminergic mechanisms related to GC-induced hypertension could contribute to this response to DEX, for example: increased reactivity to arginine–vasopressin (Iijima and Malik, 1988), renin–angiotensin system activation (Sato et al., 1994); reduction of vasodilator gene expression such as cyclohydroxylase 1 and inducible nitric oxide synthase (Qiu and Baylis, 2000; Mitchell et al., 2003); and production of reactive oxidative species (Mondo et al., 2006). The gene discussed is NOS2; the disease is hypertensive disorder.