Do the urinary bladder and large bowel interact, in sickness or in health?: ICI‐RS 2011

Abstract

Normal functioning of the urinary bladder and the distal gut is an essential part of daily physiological activity coordinated by the peripheral and central nervous systems. Pathological changes in one of these organs may induce the development of cross-organ sensitization in the pelvis and underlie clinical co-morbidity of genitourinary and GI dysfunctions. Experimental human and animal data suggest that the bladder and distal colon interact under both normal and pathological conditions, however, the directions of these interactions can change dramatically depending on the nature and duration of the applied stimuli. This review article aimed to summarize the clinical data on colon-bladder cross-reflexes in healthy individuals, as well as in patients with co-morbid disorders. It also discusses currently used animal models, experimental approaches, and suggested mechanisms of colon-bladder cross-talk. Additionally, it provides an overview of the potential pharmacological targets to develop treatment options for patients with co-morbid disorders. Presented work resulted from the discussion of colon/bladder interactions during “Think Tank 9” presentations at the International Consultation on Incontinence Research Society meeting held in Bristol, UK, 2011.

Pelvic organ cross-sensitization to enhance bladder and urethral pain behaviors in rats with experimental colitis

“…These results indicate that pain hypersensitivity of the bladder and urethra in rats with TNBS-induced colon inflammation is produced by the indirect mechanisms in the lower urinary tract other than inflammatory changes directly elicited by TNBS administered into the colon. Previous studies have demonstrated that pelvic organ cross sensitization is induced by activation of dichotomized afferents innervating different pelvic organs and that activation of nociceptive C-fiber afferents in one organ could sensitize afferent pathways in another organ to release neuropeptides such as substance P that trigger neurogenic inflammation and mast cell activation (Malykhina et al, 2012;Fitzgerald et al, 2013). Also, Pan et al demonstrated that desensitization of TRPV1-expressing afferent pathways by intracolonic application of RTx, a TRPV1 receptor agonist, prior to the induction of colonic inflammation prevented the release of these peptides from the peripheral nerve terminals and reduced the development of neurogenic cross-talk between the colon and bladder (Pan et al, 2010).…”

Does central sensitization help explain idiopathic overactive bladder?

“…Viscero-visceral hyperalgesia can occur between any two visceral organs with common innervation arising from sensory projections with overlapping or common origins in the spinal cord 75 ; visceral organ crosstalk involving the bladder is best described relative to activation of the bowel, which shares sensory innervation in regions of the thoracic and sacral spinal cord with the bladder. Convergent neural mechanisms of activation of the bladder and the bowel, in particular, explain the reproducible interactions demonstrated in experimental models (known as pelvic organ crosstalk) 73,76,77 . For instance, in animal studies, rectal stimulation either through distension 78,79 or inflammation 80 precipitates detrusor inhibition and/or overactivity that is mediated by activation of convergent bladder and bowel C-fibre afferent nerves in the spinal cord 78 .…”

Neural Control of the Lower Urinary Tract

“…For example, 3% to 15% of dorsal root ganglion (DRG) neurons are double labeled following injections of different tracers into the colon and bladder (113, 321, 400, 401). The double labeling occurs more frequently in rostral lumbar (L1–L2) than in caudal lumbosacral (L6–S1) DRG, which provide the major innervation to the bladder and colon.…”