Angiotensin (Ang) II mediates pathophysiologial changes in the kidney. Ang-(1-7) by interacting with the G protein-coupled receptor Mas may also have important biological activities. In this study, renal deficiency for Mas diminished renal damage in models of renal insufficiency as unilateral ureteral obstruction and ischemia/reperfusion injury while the infusion of Ang-(1-7) to wild-type mice pronounced the pathological outcome by aggravating the inflammatory response. Mas deficiency inhibited NF-κB activation and thus the elevation of inflammation-stimulating cytokines, while Ang-(1-7) infusion had proinflammatory properties in experimental models of renal failure as well as under basal conditions. The Ang-(1-7)-mediated NF-κB activation was Mas dependent but did not involve Ang II receptors. Therefore, the blockade of the NF-κB-activating properties of the receptor Mas could be a new strategy in the therapy of failing kidney.

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Persistent URL dx.doi.org/10.1371/journal.pone.0005406, hdl.handle.net/1765/24983
Citation
Esteban, V, Heringer-Walther, S, Sterner-Kock, A, de Bruin, R.W.F, van den Engel, S, Wang, Y, … Walther, T. (2009). Angiotensin-(1-7) and the G protein-coupled receptor Mas are key players in renal inflammation. PLoS ONE, 4(4). doi:10.1371/journal.pone.0005406