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editorial

. 2014 May 30;92(8):793–795. doi: 10.1007/s00109-014-1172-z

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© Springer-Verlag Berlin Heidelberg 2014

This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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Fig. 1 — Ang 1–7 (Asp-Arg-Val-Tyr-Ile-His-Pro), which can be formed either by the carboxypeptidase activity of ACE2 on Ang II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe) or by endopeptidase cleavage of Ang I (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu) by neprilysin (NEP), antagonizes Ang II actions on cardiovascular and renal physiology. The opposing effects of Ang II and Ang 1–7 are carried out primarily via the AT1, AT2, and Mas receptors (MAS R), respectively. Ang III (Arg-Val-Tyr-Ile-His-Pro-Phe) is the principal active peptide in the brain RAS, and its formation is regulated by aminopeptidase (AP)—as largely adapted from [2]