Oxidative stress improves coronary endothelial function through activation of the pro-survival kinase AMPK

Ehtesham Shafique; Wing C. Choy; Yuhong Liu; Jun Feng; Brenda Cordeiro; Arthur Lyra; Mohammed Arafah; Abdulmounem Yassin-Kassab; Arthus V.D. Zanetti; Richard T. Clements; Cesario Bianchi; Laura E. Benjamin; Frank W. Sellke; Md. Ruhul Abid

doi:doi:http://dx.doi.org/10.18632/aging.100569

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Research Paper Volume 5, Issue 7 pp 515—530

Oxidative stress improves coronary endothelial function through activation of the pro-survival kinase AMPK

Figure 2. Increased coronary vasodilatation in Tet-OFF mice with higher EC-ROS.

(A) Endothelium-dependent dilation of coronary arterioles from Tet-ON (n=6) and Tet-OFF (n=6) NVF mice in response to VEGF. 22±3.72% increase in vasodilation in Tet-OFF vs. Tet-ON. (B) Endothelium-dependent dilation of coronary arterioles from Tet-ON (n=6) and Tet-OFF (n=6) NVF mice in response to acetylcholine (Ach). 25±2.43% increased dilation in Tet-OFF vs. Tet-ON. (C) Endothelium-independent dilation of coronary arterioles from Tet-ON (n=6) and Tet-OFF (n=6) mice in response to NO donor, SNP. (D) NO-cGMP signaling inhibitor ODQ (10 μmol/L) inhibited coronary vasorelaxation in both Tet-ON and Tet-OFF coronary vessels. n = 6/group. All coronary vessels were pre-constricted ex-vivo using U46619 prior to the addition of VEGF, Ach or SNP as indicated.