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. 2011 Jun 23;121(7):2845–2854. doi: 10.1172/JCI57324

Figure 8. The intrarenal renin-angiotensin system was altered in ptAadc–/– mice.

Figure 8

(A) Antagonism of AT1 receptors with candesartan reduced SBP in ptAadc–/– mice to levels seen in wild-type mice (*P < 0.01 vs. basal wild type, †P < 0.01 vs. basal ptAadc–/–; n = 6 in each group). (B) Ang II infusion (0.9 mg/kg/d) for 4 weeks led to more significant increases in albuminuria (*P = 0.012) and tubulointerstitial (TI) injury (†P = 0.03) in ptAadc–/– mice than wild-type mice (n = 5). ACR, albumin creatinine ratio. (C) The expression of nitrotyrosine (a marker of oxidative stress) and KIM-1 (a marker of kidney injury) was much higher in Ang II–treated ptAadc–/– mice than Ang II–treated wild-type mice. Original magnification: ×63. Quantitative image analysis indicated nitrotyrosine levels were significantly higher in Ang II–treated ptAadc–/– mice than Ang II–treated wild-type mice (*P < 0.01; n = 4). (D) There were increased mRNA levels of AT1b (*P < 0.00001) but decreased mRNA levels of AT2 (*P < 0.00001) and Mas (†P < 0.0001) in ptAadc–/– mice compared with those in wild-type mice (n = 4). (E) Immunoblotting indicated increased angiotensinogen (AGT) but decreased Mas protein levels in ptAadc–/– mice.