5. Conclusions
Our study provides evidence that H2O2, at a concentration range associated with inflammation and ischemia–reperfusion[28], enhanced SBCs of human-bladder. Activation of TRPA1 channels on peripheral sensory nerves and then the release of SP or PGE2 were important mechanism for H2O2 induced enhancing effects. Our study provides new insights for the mechanisms underlying ROS leading to OAB. Targeting TRPA1 channels might be the promising strategy for clinical treatment of OAB in conditions associated with excessive production of ROS.