15 In health, the motor innervation to the bladder is wholly dependent on the action of acetylcholine acting via M3 receptors, although this changes in disease states.
For instance, it has been suggested that nitric oxide can be released from urothelial cells upon mechanical force or stretch, mimicking bladder distension, and that this release is dependent on the presence of vanilloid receptors [ 127].
In this study, both pelvic pain and bladder pathophysiology were dependent upon mast cells.
We therefore hypothesized that tumorigenesis following loss of function of Pten in the bladder may be dependent on the activity of other mechanisms regulating mTOR.
These data demonstrate that cystitis pain and bladder pathophysiology are dependent on mast cells through the independent actions of histamine and TNF, respectively, and identify histamine receptors as therapeutic targets for direct intervention in pelvic pain of IC.
Our previous studies demonstrated that PRV-induced bladder pathophysiology was dependent upon TNF [12], [17], so we examined the role of TNF in pelvic pain responses by quantifying pelvic tactile sensitivity in TNF−/− and TNFR1/2−/− mice following PRV infection.
It was found that NGF-induced bladder overactivity was dependent on TRPV1, as TRPV1 knockout animals did not respond with detrusor overactivity to NGF treatment.
Objective: The mechanical stability of the genitourinary tract is dependent on intact collagen fibers that support the bladder neck, urethra, and pelvic organs.
The threshold is dependent to some extent on the rate of filling and is higher when filling is slow; and training affects the amount the bladder can retain.
