| Literature DB >> 20153712 |
Lucienne S Lara1, Diogo Vives, Juliana S Correa, Flavia P Cardozo, Maria Fernanda Marques-Fernades, Anibal G Lopes, Celso Caruso-Neves.
Abstract
We showed previously that angiotensin-(1-7) [Ang-(1-7)] reversed stimulation of proximal tubule Na+-ATPase promoted by angiotensin II (Ang II) through a D-ala(7)-Ang-(1-7) (A779)-sensitive receptor. Here we investigated the signaling pathway coupled to this receptor. According to our data, Ang-(1-7) produces a MAS-mediated reversal of Ang II-stimulated Na+-ATPase by a Gs/PKA pathway because: (1) the Ang-(1-7) effect is reversed by GDPbetaS, an inhibitor of trimeric G protein and Gs polyclonal antibody. Cholera toxin, an activator of Gs protein, mimicked it; (2) in the presence of Ang II, Ang-(1-7) increased the PKA activity 10-fold; (3) the peptide inhibitor of PKA blocked the Ang-(1-7) effect on Ang II-stimulated Na+-ATPase; (4) Ang-(1-7) reverses the Ang II-stimulated PKC activity; (5) cAMP mimicked the Ang-(1-7) effect on the Ang II-stimulated Na+-ATPase. Our results provide new understanding about the signaling mechanisms coupled to MAS receptor-mediated renal Ang-(1-7) effects. 2010 Elsevier Inc. All rights reserved.Entities:
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Year: 2010 PMID： 20153712 DOI： 10.1016/j.abb.2010.02.005
Source DB: PubMed Journal: Arch Biochem Biophys ISSN： 0003-9861 Impact factor: 4.013