<p>Western blots showed that AngII treatment (100 nmol/L, 24 h) decreased ACE2 (A; 100 KDa, n = 6, **<i>P</i><0.01 vs. vehicle), increased AT1R (43 KDa; B; n = 6, *<i>P</i><0.05 vs. vehicle) without changing AT2R (44 KDa; C; <i>P</i>>0.05 vs. vehicle) protein expression. Representative DHE staining (D) and quantified data (E), showing that AngII (100 nmol/L, 30 min) significantly increased ROS production (n = 6, **<i>P</i><0.01 vs. no treatment). Pre-treatment with Ad-ACE2-eGFP reduced AngII-stimulated ROS formation (n = 6, †<i>P</i><0.05 vs. AngII+Ad-eGFP, *<i>P</i><0.05 vs. no treatment). Blockade of AT1R with losartan completely prevented AngII-mediated ROS production (n = 6, †<i>P</i><0.05 vs. AngII+Ad-eGFP).</p
