Renal deficiency for the Mas receptor diminished renal damage in models of renal insufficiency, while infusion of Angiotensin-(1-7) aggravated the inflammatory response via Mas-dependent NF-kB activation.
Does Mas receptor deficiency or Ang-(1-7) infusion affect renal inflammation and damage in mouse models of renal insufficiency?
Blockade of the NF-kappaB-activating properties of the Mas receptor could be a potential therapeutic strategy for renal failure.
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-kappaB 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-kappaB activation was Mas dependent but did not involve Ang II receptors. Therefore, the blockade of the NF-kappaB-activating properties of the receptor Mas could be a new strategy in the therapy of failing kidney.
Esteban et al. (Wed,) conducted a other in Renal Inflammation. Angiotensin-(1-7) infusion and Mas receptor deficiency vs. Saline infusion and wild-type controls was evaluated on Renal inflammation and pathomorphological changes. Renal deficiency for the Mas receptor diminished renal damage in models of renal insufficiency, while infusion of Angiotensin-(1-7) aggravated the inflammatory response via Mas-dependent NF-kB activation.