Skip to main content
. 2019 Aug 27;10:586. doi: 10.3389/fendo.2019.00586

Figure 4.

Figure 4

GPER activation prevented Ang II-induced increases in ROS and NADP/NADPH ratio. (A) Stimulation of A7r5 cells with 100 nM Ang II for 4 h significantly increased ROS, which was prevented by pretreatment with the GPER agonist G-1 for 24 h. 1-way ANOVA, p = 0.0004, Tukey **p < 0.01 vs. vehicle (Veh); ###p < 0.0001 vs. Ang II. (B) Ang II-induced increases in the NADP/NADPH ratio were also mitigated by G-1. Kruskai-Wallis test, p < 0.0001, Dunn, ***p < 0.001 vs. Veh; ###p < 0.001 vs. Ang II. (C) Ang II also increased NADP/NADPH ratio in primary male and female Sprague Dawley rat aortic smooth muscle cells, which was reversed by G-1. 2-way ANOVA with Geisser-Greenhouse correction, *p < 0.0323 for interaction, Tukey, *p < 0.05 vs. Veh; #p < 0.05 vs. Ang II; †p < 0.01 sex effect. (D) The GPER antagonist G36 blocked the ability of G-1 to inhibit Ang II effects on NADP/NADPH ratio. 1-way ANOVA, p < 0.0001, Tukey, **p < 0.01 vs. Veh. (E) The increase in NADP/NADPH ratio induced by Ang II was completely prevented by losartan (Los). 1-way ANOVA, p < 0.0001, Tukey, ***p < 0.001 vs. vehicle; ###p < 0.001 vs. Ang II.