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. 2020 Sep 30;11:566410. doi: 10.3389/fphys.2020.566410

Figure 2.

Figure 2

The AngII/AT1R pathway reduces the levels of eNOS Ser1177 phosphorylation and NO production by activating protein phosphatase 2A (PP2A). (A) AngII augmented PP2A activity, while CAN blocked AngII-mediated enhancement of PP2A activity. HUVECs were pretreated with 10−6 M CAN for 3 h or not, then stimulated with 10−7 M AngII for 12 h (n = 4 independent experiments). (B) PP2A activity was increased in the mesenteric arteries of AngII-infused rats. CAN blocked AngII-induced upregulation of PP2A activity (n = 3 rats per group). (C,D) PP2A inhibitor (OA) blocked the effect of AngII on eNOS Ser1177 in vitro. HUVECs were pretreated with 10−8 M OA for 1 h or not, then stimulated with 10−7 M AngII for 12 h (n = 6 independent experiments). (E,F) OA blocked AngII-induced downregulation of NO production in HUVECs (200× magnification; n = 4 independent experiments). *p < 0.05 vs. Control or Sham group; #p < 0.05 vs. AngII group.