Angiotensin II type 2 receptor deficiency aggravates renal injury and reduces survival in chronic kidney disease in mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2009-05

AUTHORS

Ralf A Benndorf, Christian Krebs, Birgit Hirsch-Hoffmann, Edzard Schwedhelm, Gabriele Cieslar, Robin Schmidt-Haupt, Oliver M Steinmetz, Catherine Meyer-Schwesinger, Friedrich Thaiss, Munif Haddad, Susanne Fehr, Andreas Heilmann, Udo Helmchen, Lutz Hein, Heimo Ehmke, Rolf A Stahl, Rainer H Böger, Ulrich O Wenzel

ABSTRACT

Angiotensin II (Ang II) activates at least two receptors, AT1 and AT2, with the majority of its effects-such as vasoconstriction, inflammation, and matrix deposition-mediated by the AT1 receptor. It is thought that the AT2 receptor counteracts these processes; however, recent studies have found proinflammatory and hypertrophic effects of this receptor subtype. To identify the physiological roles of the AT2 receptor in chronic kidney disease, we performed renal ablation in AT2 receptor knockout and wild-type mice. Renal injury caused a greater impairment of renal function, glomerular injury, albuminuria, and mortality in the knockout mice than in the wild-type mice. There was increased fibronectin expression and inflammation in the knockout mice, as shown by augmented monocyte/macrophage infiltration and higher chemokine monocyte chemotactic protein-1 (MCP-1) and RANTES expression in the remnant kidney. The higher mortality and renal morbidity of the knockout mice was not due to differences in systemic blood pressure, glomerular volume, AT1 receptor, renin, or endothelial nitric oxide synthase expression. Whether activation of the AT2 receptor will have therapeutic benefit in chronic kidney disease will require further study. More... »

PAGES

1039-1049

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ki.2009.2

DOI

http://dx.doi.org/10.1038/ki.2009.2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1029506534

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19212419


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