Fig. 3.

RAS: A classic model of RAS showing deleterious and protective effects. The precursor peptide AGT is cleaved by renin to form the Ang I, which is then cleaved by ACE to form Ang II. Ang II is the main peptide of RAS and exerts it effects by binding to two GPCRs AT₁ receptor and AT₂ receptor. Binding of Ang II to AT₁ receptor stimulates vasoconstrictive/pro-inflammatory pathways, whereas its binding to AT₂ receptor activates the vasodilative/anti-inflammatory signaling. Ang II is further cleaved by ACE2 to Ang (1–7), which binds to Mas receptor and promotes vasodilative/anti-inflammatory effects. Ang (1–7) can also be generated directly from Ang I by the action of neprilysin (Nep) or by the action of ACE2 on Ang I to form Ang (1–9), which is subsequently cleaved to generate Ang (1–7) through Nep.