A Novel Mechanism of Action for Angiotensin-(1–7) via the Angiotensin Type 1 Receptor
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Angiotensin-(1–7) (Ang-[1–7]) was originally thought to be an inactive metabolite of Ang II in the renin–angiotensin system (RAS). However, reported biological effects and seminal discoveries of an angiotensin-converting enzyme (ACE) homolog, ACE2 that metabolises Ang II to Ang-(1–7),1 combined with identification of the G-protein–coupled receptor Mas as an endogenous Ang-(1–7) receptor2 defined a natural counter-regulatory ACE2/Ang-(1–7)/Mas axis of the RAS. The counter-regulatory axis of the RAS is firmly established to inhibit detrimental effects mediated through the classical ACE/Ang II/angiotensin type 1 receptor (AT1R) axis (Figure). Moreover, it is simplistic to separate the RAS into these 2 axes because the systemic and local tissue-specific RAS includes a wide range of molecules with biological action, including the alternative Ang II receptor, the angiotensin type 2 receptor (AT2R), other peptide metabolites, for example, Ang-(1–9), Ang III, and Ang IV, and recent discoveries including an Ang-(1–7) metabolite, alamandine, and its receptor Mas-related G-protein–coupled receptor D.3