Experimental models of MR-dependent hypertension (deoxycorticosterone acetate/salt and aldosterone/salt rodents) exhibit oxidative stress as evidenced by increased Nox expression/activity, increased vascular ROS production, and elevated levels of TBARS, effects that are ameliorated by treatment with MR antagonists.122, 123, 124, 125. The gene discussed is NR3C2; the disease is substance dependence.