Multiple signal transduction pathways are involved in hydrogen peroxide‐induced contraction in rat thoracic aorta and vena cava

The membrane permeable reactive oxygen species hydrogen peroxide (H 2 O 2 ) causes vascular contraction and relaxation. We previously observed that H 2 O 2 contracted rat thoracic aorta and vena cava. When K + channel activity was impaired, aortic H 2 O 2 ‐induced contraction was potentiated. The focus of this study was to compare the signal transduction pathways involved in H 2 O 2 ‐induced contraction in vena cava under quiescent conditions and in aorta contracted with KCl (30 mM) to inhibit K + channel activity. We hypothesized that the signal transduction pathways mediating H 2 O 2 ‐induced contraction in vena cava under quiescent conditions would differ from those mediating H 2 O 2 ‐induced contraction in aorta contracted with KCl (30 mM). The TXA 2 receptor antagonist, ICI‐185282 (ICI, 10 μM), nearly abolished maximal aortic and venous H 2 O 2 ‐induced contraction (aorta ICI: 100% reduction in maximum H 2 O 2 ‐induced contraction; vena cava ICI: 80% reduction). The p38 MAPK inhibitor SB‐203580 (SB, 10 μM) and an Erk MAPK inhibitor, PD‐98059 (PD, 10 μM), reduced maximal aortic and venous H 2 O 2 ‐induced contraction (aorta SB: 63% reduction in maximum H 2 O 2 ‐induced contraction; aorta PD: 80% reduction; vena cava SB: 91% reduction; vena cava PD: 100% reduction). We conclude that multiple signal transduction pathways specifically TXA 2 receptors, Erk MAPK, p38 MAPK and Rho kinase ‐ demonstrated in previous experiments ‐ mediate H 2 O 2 ‐induced contraction and that within the context of these pathways, there are no differences in contractile pathways utilized by H 2 O 2 in arteries and veins.