In the central nervous system, Ang II acting on AT1R results in cardiac baroreflex desensitization and resetting, increased sympathetic outflow, vasopressin release, and stimulation of the water intake, leading to the increase in blood pressure [13] . It has been shown that upregulated AGT, ACE, Ang II, and AT1R in the brain are involved in the development and maintenance of hypertension and heart failure [7, 14] . Similar to the observations in the periphery, Ang-(1-7) shows opposite properties to Ang II in the central nervous system, serving as an important neuromodulator in the central control of cardiovascular function. It has been well demonstrated that central Ang-(1-7) increases cardiac baroreflex sensitivity [15, 16] , reduces norepinephrine release [17] and decreases blood pressure [18, 19] in hypertensive rats. The depressor effects of Ang-(1-7) in the brain have also been shown to be mediated by increase in bradykinin levels [20] , potentiating the hypotensive effects of bradykinin [21] and stimulating nitric oxide (NO) release [22] . ACE2 provides an important route for the metabolism of Ang II and, as the principal forming enzyme for Ang-(1-7), shifts the balance between the two biological active peptides.