Chronic pelvic pain of unknown etiology is a common clinical condition and may develop as a result of cross-sensitization in the pelvis. The aim of the current study was to compare transient receptor potential vanilloid 1 (TRPV1) activated pathways on detrusor contractility in vivo and in vitro using a rat model of pelvic organ cross-sensitization. Animals (Sprague-Dawley rats) received intracolonic saline (control), resiniferatoxin (RTX, 10-7 M), 2,4,6-trinitrobenzene sulfonic acid (TNBS) or double treatment (RTX followed by TNBS). Detrusor muscle contractility was assessed in vitro and in vivo. Intracolonic RTX increased the contractility of the isolated detrusor in response to electric field stimulation (EFS) by two-fold (p≤0.001) and enhanced the contractility of bladder smooth muscle to carbachol (CCh). Acute colonic inflammation reduced detrusor contractility upon application of CCh in vitro; decreased bladder capacity by 28.1% (p≤0.001) and reduced micturition volume by 60% (p≤0.001). These changes were accompanied by an increased number of non-micturition contractions from 3.7±0.7 to 15±2.7 (N=6 in both groups, p≤0.001 to control). Desensitization of TRPV1 receptors prior to the induction of acute colitis restored the response of isolated detrusor strips to CCh but not to EFS stimulation. Cystometric parameters were significantly improved in animals with double treatment. Our data suggest that acute colonic inflammation triggers the occurrence of detrusor instability via activation of TRPV1 related pathways. Comparison of the results obtained under in vitro vs in vivo conditions provides evidence that intact neural pathways are critical for the development of an overactive bladder resulted from pelvic organ cross-talk.
- neurogenic inflammation
- chronic pelvic pain
- Copyright © 2010, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology