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Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT1 receptor with protective action in cardiac hypertrophy

Teixeira, Larissa B. ; Parreiras-e-Silva, Lucas T. ; Bruder-Nascimento, Thiago ; Duarte, Diego A. ; Simões, Sarah C. ; Costa, Rafael M. ; Rodríguez, Deisy Y. ; Ferreira, Pedro A. B. ; Silva, Carlos A. A. ; Abrao, Emiliana P. ; Oliveira, Eduardo B. ; Bouvier, Michel ; Tostes, Rita C. ; Costa-Neto, Claudio M.

Scientific reports, 2017-09, Vol.7 (1), p.1-10, Article 11903 [Periódico revisado por pares]

London: Nature Publishing Group

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Título:
Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT1 receptor with protective action in cardiac hypertrophy
Autor: Teixeira, Larissa B. ; Parreiras-e-Silva, Lucas T. ; Bruder-Nascimento, Thiago ; Duarte, Diego A. ; Simões, Sarah C. ; Costa, Rafael M. ; Rodríguez, Deisy Y. ; Ferreira, Pedro A. B. ; Silva, Carlos A. A. ; Abrao, Emiliana P. ; Oliveira, Eduardo B. ; Bouvier, Michel ; Tostes, Rita C. ; Costa-Neto, Claudio M.
Assuntos: Angiotensin ; Angiotensin II ; Arrestin ; Biochemistry ; Blood pressure ; Competition ; Endocrine system ; Enzymes ; Heart ; Heart diseases ; Hypertrophy ; Immunology ; Kinases ; Ligands ; Proteins ; Renin ; Sodium ; Vasoconstriction ; Ventricle
É parte de: Scientific reports, 2017-09, Vol.7 (1), p.1-10, Article 11903
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: 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 hypertrophy, we show that Ang-(1-7) significantly attenuates heart hypertrophy by reducing both heart weight and ventricular wall thickness and the increased end-diastolic pressure. Whereas neither the single blockade of AT1 or Mas receptors with their respective antagonists prevented the cardioprotective action of Ang1-7, combination of the two antagonists partially impaired the effect of Ang-(1-7). Taken together, these data indicate that Ang-(1-7) mediates at least part of its cardioprotective effects by acting as an endogenous β-arrestin-biased agonist at the AT1R.
Editor: London: Nature Publishing Group
Idioma: Inglês

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Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT1 receptor with protective action in cardiac hypertrophy

London: Nature Publishing Group

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