Classically, the RAS involves the conversion of angiotensinogen by renin into angiotensin I (Ang I). Ang I is metabolized to Ang II via the dipeptide carboxypeptidase ACE. The pro-inflammatory effects of Ang II (7, 8, 9) are mediated through Ang II type I (AT1) receptors. Recently, the ACE2 receptor and its signaling pathway were identified as an important counter regulatory mechanism to the classic RAS.