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.