Fig. 3.

Molecular mechanisms of enhanced H₂O₂/EDH factor-mediated responses in microvesseles. Multiple mechanisms are involved in the enhanced EDH-mediated responses in microvessels. AMPKα₁, α₁-subunit of AMP-activated protein kinase; CaM, calmodulin; CaMKKβ, Ca²⁺/CaM-dependent protein kinase β; CaMK2, Ca²⁺/CaM dependent protein kinase II; cGMP, cyclic GMP; Cu,Zn-SOD, copper-zinc superoxide dismutase; EDH, endothelium-dependent hyperpolarization; H₂O₂, hydrogen peroxide; IP₃, inositol trisphosphate; I/R, ischemia-reperfusion; K_Ca, calcium-activated potassium channel; NO, nitric oxide; NOSs, NO synthases; P, phosphorylation; PKG1α, 1α-subunit of protein kinase G; PLC, phospholipase C; sGC, soluble guanylate cyclase; TRPV4, transient receptor potential vanilloid 4, VSMC; vascular smooth muscle cells.