Angiotensin (Ang)-converting enzyme (ACE) 2 cleaves Ang-II into the vasodilator 
peptide Ang-(1-7), thus acting as a pivotal element in balancing the local 
effects of these peptides. ACE2 has been identified in various tissues and is 
supposed to be a modulator of cardiovascular function. Decreases in ACE2 
expression and activity have been reported in models of hypertension, heart 
failure, atherosclerosis, diabetic nephropathy and others. In addition, the 
expression level and/or activity are affected by other renin-angiotensin system 
components (e.g., ACE and AT1 receptors). Local inhibition or global deletion of 
brain ACE2 induces a reduction in baroreflex sensitivity. Moreover, ACE2-null 
mice have been shown to exhibit either blood pressure or cardiac dysfunction 
phenotypes. On the other hand, over-expression of ACE2 exerts protective effects 
in local tissues, including the brain. In this review, we will first summarize 
the major findings linking ACE2 to cardiovascular function in the periphery then 
focus on recent discoveries related to ACE2 in the CNS. Finally, we will unveil 
new tools designed to address the importance of central ACE2 in various 
diseases, and discuss the potential for this carboxypeptidase as a new target in 
the treatment of hypertension and other cardiovascular diseases.