We found that the overexpression of MnSOD attenuated the angiotensin II-induced pressor response and also suppressed the angiotensin II-induced oxidative stress production in the RVLM (Nozoe et al., 2008) A recent study also demonstrated that the oxidative stress-induced impairment of the mitochondrial electron transport chain complexes in the RVLM contribute to further chronic oxidative stress, thereby leading to augmented central sympathetic outflow and hypertension (Chan et al., 2009). This evidence concerns the gene AGT and hypertensive disorder.