Research Paper Volume 5, Issue 7 pp 515—530
Oxidative stress improves coronary endothelial function through activation of the pro-survival kinase AMPK
Figure 4. Inhibition of AMPK signaling reduced coronary vasodilatation in Tet-OFF NVF but not in Tet-ON NVF.
(A) Isolated coronary vessels from Tet-ON and Tet-OFF transgenic mice (n=6/group) were subject to microvessel reactivity assay in the presence or absence of Compound C (80 μmol/L). Ach-mediated vasodilatation was inhibited by Compound C in the coronary vessels from Tet-OFF mice, whereas Compound C had no significant effect on the coronary vessels from Tet-ON mice. (B) Same as in (A), except pre-treatment was carried out using CaMKKβ-inhibitor STO-609 (50 nmol/L).