Several studies have focused on the mechanisms involved in ACE2 regulation of blood pressure and other cardiovascular functions. Baroreflex sensitivity and autonomic function are important central mechanisms modulating blood pressure and other cardiovascular functions. It has been shown that inhibition of ACE2 activity in the NTS, by injecting a specific inhibitor in this region, reduces the sensitivity of the baroreceptor reflex control of heart rate to increases in arterial pressure [29•] . Similarly, we previously showed that ACE2 gene deletion on a C57bl/6 background mouse resulted in impairment of the spontaneous baroreflex sensitivity (SBRS), increased sympathetic tone, and decreased parasympathetic tone [40, 41] . Moreover, exercise training-induced increase in endogenous ACE2 in the brain of CHF rabbits was associated with an attenuation of sympathetic nerve activity in these animals [34] . Also, overexpressing ACE2 in the PVN, by virus-mediated gene transfer, improves renal sympathetic nerve activity in coronary ligation-induced CHF rats [42] . Global overexpression of ACE2 in the brain also restored the impaired SBRS, normalized the increased sympathetic tone, and decreased parasympathetic tone in transgenic hypertensive mice, contributing to the attenuation of hypertension in these animals [31••]. In low-dose Ang II infusion, a model of neurogenic hypertension, although ACE2 overexpression in the brain did not alter the increased sympathetic tone, it significantly prevented the decrease in both SBRS and parasympathetic tone and attenuated the development of hypertension [33••]. Similar observations were made by Gao et al. [43] showing that global overexpression of exogenous ACE2 in the brain prevents impairment of baroreflex sensitivity and sympathoexcitation in the CHF state.