Premium
Do we understand any more about bladder interstitial cells?—ICI‐RS 2013
Author(s) -
Kanai Anthony,
Fry Christopher,
HannaMitchell Ann,
Birder Lori,
Zabbarova Irina,
Bijos Dominika,
Ikeda Youko
Publication year - 2014
Publication title -
neurourology and urodynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 90
eISSN - 1520-6777
pISSN - 0733-2467
DOI - 10.1002/nau.22591
Subject(s) - medicine , interstitial cell of cajal , interstitial cystitis , urothelium , spinal cord injury , lamina propria , urinary bladder , reflex , urination , urology , spinal cord , overactive bladder , interstitial cell , detrusor muscle , urinary incontinence , urinary system , anatomy , smooth muscle , pathology , alternative medicine , psychiatry , epithelium
Aims To present a brief review on discussions from “Do we understand any more about lower urinary tract interstitial cells?” session at the 2013 International Consultation on Incontinence‐Research Society (ICI‐RS) meeting in Bristol, UK. Methods Discussion focused on bladder interstitial cell (IC) subtypes, their localization and characterization, and communication between themselves, the urothelium, and detrusor smooth muscle. The role of ICs in bladder pathologies and new methods for studying ICs were also addressed. Results ICs have been studied extensively in the lower urinary tract and have been characterized based on comparisons with ICs of Cajal in the gastro‐intestinal tract. In fetal bladders it is believed that ICs drive intrinsic contractions to expel urine through the urachus. These contractions diminish postpartum as bladder innervation develops. Voiding in human neonates occurs when filling triggers a spinal cord reflex that contracts the detrusor; in rodents, maternal stimulation of the perineum triggers voiding. Following spinal cord injury, intrinsic contractions, and spinal micturition reflexes develop, similar to those seen during neonatal development. These enhanced contractions may stimulate nociceptive and mechanosensitive afferents contributing to neurogenic detrusor overactivity and incontinence. The IC‐mediated activity is believed to be initiated in the lamina propria by responding to urothelial factors. These IC may act syncytially through gap junction coupling and modulate detrusor activity through unknown mechanisms. Conclusion There has been a great deal of information discovered regarding bladder ICs, however, many of their (patho)physiological functions and mechanisms are still unclear and necessitates further research. Neurourol. Urodynam. 33:573–576, 2014 . © 2014 Wiley Periodicals, Inc.