PMC:7161517 / 8808-9732 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7161517","sourcedb":"PMC","sourceid":"7161517","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7161517","text":"Angiotensinogen is converted to angiotensin I (Ang I) via renin. Ang I is converted to Ang II via angiotensin-converting enzyme (ACE), which also hydrolyzes bradykinin into its inactive metabolites, promoting inflammation. The pro-inflammatory effects of Ang II are mediated by Ang II type I receptor (AT1), which stimulates aldosterone secretion from the adrenal medulla and antidiuretic hormone from the posterior pituitary. Aldosterone decreases membrane ACE2 expression. Endothelin-1 inhibits angiotensin 1-7 (Ang1-7) via extracellular signal-regulated kinase (ERK)1/ERK2 pathways. Ang II, under favorable conditions (dashed line), can be converted to Ang1-7 via ACE2, whose counter regulatory effects are mediated by the Mas receptor. Ang1-7 can also be formed via conversion of Ang I to an intermediate Ang1-9 or directly via zinc metallopeptidase neprilysin/prolyl endopeptidase (PEP). 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