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.

Additional Metadata
Persistent URL,
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