Moxibustion attenuates neurogenic detrusor overactivity in spinal cord injury rats by inhibiting M2/ATP/P2X3 pathway

Abstract Background Activation of muscarinic receptors located in bladder sensory pathways is generally considered to be the primary contributor for driving the pathogenesis of neurogenic detrusor overactivity following spinal cord injury. The present study is undertaken to examine whether moxibustion improves neurogenic detrusor overactivity via modulating the abnormal muscarinic receptor pathway. Methods Female Sprague-Dawley rats were subjected to spinal cord injury with T9-10 spinal cord transection. Fourteen days later, animals were received moxibustion treatment for one week. Urodynamic parameters and pelvic afferents discharge were measured. Acetylcholine and adenosine triphosphate content in the voided cystometry fluid were determined. Expressions of M2, M3 and P2X3 receptor in the bladder mucosa were evaluated. Results Moxibustion treatment prevented the development of detrusor overactivity in SCI rats, with an increase in the intercontraction interval and micturition pressure threshold and a decrease in afferent activity during filling. The expression of M2, but not M3, was markedly suppressed by moxibustion, accompanied by a reduction in the level of ATP and P2X3. M2 receptor antagonist methoctramine hemihydrate had similar effects to moxibustion on bladder function and afferent activity, while the M2-preferential agonist oxotremorine methiodide abolished the beneficial effects of moxibustion. Conclusions Moxibustion is a potential candidate for treatment of neurogenic bladder overactivity in a rat model of spinal cord injury possibly through inhibiting the M2/ATP/P2X3 pathway.