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. 2020 Sep 24;24(22):13093–13103. doi: 10.1111/jcmm.15914

Figure 2.

Figure 2

Double deletion of angiotensin (Ang)‐converting enzyme‐2 (ACE2) and Mas receptor enhances Ang II‐induced hypertension and hypertensive renal injury. A, Systolic blood pressure (SBP) at weeks 1, 2, 3, and 4. B, 24‐hour proteinuria. C, Serum creatinine (Scr). D, Creatinine clearance rate (Ccr). E, Renal periodic acid Schiff (PAS) staining at week 4 after Ang II infusion. Glomerular mesangial matrix expansion was scored. Data represent the mean ± SEM for groups of 6‐15 mice. *P < .05, **P < .01, ***P < .001 vs. WT + saline (WT + SL); # P < .05, ## P < .01, ### P < .001 vs. WT + Ang II; $ P < .05, $$ P < .01, $$$ P < .001 vs. ACE2 KO + Ang II and Mas KO + Ang II. Scale bar, 50 μm. WT + SL represents wild‐type (WT) mice received saline infusion; WT + Ang II represents WT mice received Ang II infusion; ACE2 KO + Ang II represents ACE2 KO mice received Ang II infusion; Mas KO + Ang II represents Mas KO mice received Ang II infusion and A/M KO + Ang II represents mice with double deletion of ACE2 and Mas received Ang II infusion