Figure 2.

BTA dampens afferent input. This occurs by both direct (blocking of ATP release in response to stretch), and indirect mechanisms (normalizing NO release, while preventing increased TRPV1/P2X3 receptor expression and NGF-mediated increase in excitability and innervation density). Increased NO release may act via myofibroblasts to attenuate afferent activity. However, the effects of BTA on NO release may be context-dependent, varying among LUT disorders. BTA, botulinum toxin A; NGF, nerve growth factor; ATP, adenosine triphosphate; ACh, acetylcholine; NO, nitric oxide.