biostudies-literatureUnknown7(1)Teixeira LBCIHRThe renin-angiotensin system (RAS) plays a key role in the control of vasoconstriction as well as sodium and fluid retention mediated mainly by angiotensin (Ang) II acting at the AT₁ receptor (AT1R). Ang-(1-7) is another RAS peptide, identified as the endogenous ligand of the Mas receptor and known to counterbalance many of the deleterious effects of AngII. AT1R signaling triggered by β-arrestin-biased agonists has been associated to cardioprotection. Because position 8 in AngII is important for G protein activation, we hypothesized that Ang-(1-7) could be an endogenous β-arrestin-biased agonist of the AT1R. Here we show that Ang-(1-7) binds to the AT1R without activating Gq, but triggering β-arrestins 1 and 2 recruitment and activation. Using an in vivo model of cardiac hypertrScientific reports11903https://www.ebi.ac.uk/biostudies/studies/S-EPMC5605686biostudies-literatureAng-(1-7) is an endogenous β-arrestin-biased agonist of the AT₁ receptor with protective action in cardiac hypertrophy.PMC5605686Oliveira EBParreiras-E-Silva LTDuarte DABouvier MCosta RMSimoes SCSilva CAAFerreira PABAbrao EPRodriguez DYCosta-Neto CMTeixeira LBBruder-Nascimento TTostes RCfalseAng-(1-7) is an endogenous β-arrestin-biased agonist of the AT₁ receptor with protective action in cardiac hypertrophy.The renin-angiotensin system (RAS) plays a key role in the control of vasoconstriction as well as sodium and fluid retention mediated mainly by angiotensin (Ang) II acting at the AT₁ receptor (AT1R). Ang-(1-7) is another RAS peptide, identified as the endogenous ligand of the Mas receptor and known to counterbalance many of the deleterious effects of AngII. AT1R signaling triggered by β-arrestin-biased agonists has been associated to cardioprotection. Because position 8 in AngII is important for G protein activation, we hypothesized that Ang-(1-7) could be an endogenous β-arrestin-biased agonist of the AT1R. Here we show that Ang-(1-7) binds to the AT1R without activating Gq, but triggering β-arrestins 1 and 2 recruitment and activation. Using an in vivo model of cardiac hypertr2017-01-01T00:00:00Z2017 Sep2025-04-19T03:33:04.338Z2019-03-27T02:56:52ZS-EPMC56056862892841010.1038/s41598-017-12074-3