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International Journal of Hypertension
Volume 2012, Article ID 808726, 8 pages
http://dx.doi.org/10.1155/2012/808726
Research Article

Renoprotective Effects of AVE0991, a Nonpeptide Mas Receptor Agonist, in Experimental Acute Renal Injury

1Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, UFMG, 31270-901 Belo Horizonte, MG, Brazil
2Departamento de Fisiologia e Biofísica, Instituto de Ciências Biológicas, UFMG, 31270-901 Belo Horizonte, MG, Brazil
3Departamento de Cirurgia, Faculdade de Medicina, UFMG, 30130-100 Belo Horizonte, MG, Brazil
4Max Delbrück Center for Molecular Medicine, Berlin Buch, 13092 Berlin, Germany
5Departamento de Patologia Geral, Instituto de Ciências Biológicas, UFMG, 31270-901 Belo Horizonte, MG, Brazil
6Departamento de Microbiologia, Instituto de Ciências Biológicas, UFMG, 31270-901 Belo Horizonte, MG, Brazil
7Departamento de Pediatria, Faculdade de Medicina, UFMG, 30130-100 Belo Horizonte, MG, Brazil

Received 30 August 2011; Accepted 21 October 2011

Academic Editor: Anderson J. Ferreira

Copyright © 2012 Lívia Corrêa Barroso et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Renal ischemia and reperfusion (I/R) is the major cause of acute kidney injury in hospitalized patients. Mechanisms underlying reperfusion-associated injury include recruitment and activation of leukocytes and release of inflammatory mediators. In this study, we investigated the renal effects of acute administration of AVE0991, an agonist of Mas, the angiotensin-(1–7) receptor, the angiotensin-(1–7) receptor, in a murine model of renal I/R. Male C57BL/6 wild-type or Mas−/− mice were subjected to 30 min of bilateral ischemia and 24 h of reperfusion. Administration of AVE0991 promoted renoprotective effects, as seen by improvement of function, decreased tissue injury, prevention of local and remote leucocyte infiltration, and release of the chemokine, CXCL1. I/R injury was similar in WT and Mas−/− mice, suggesting that endogenous activation of this receptor does not control renal damage under baseline conditions. In conclusion, pharmacological interventions using Mas receptor agonists may represent a therapeutic opportunity for the treatment of renal I/R injury.