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1 Department of Cell Biology and Physiology, University of Pittsburgh, Pittsburgh, PA, USA
2 Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA
3 Department of Pharmacology, University of Pittsburgh, Pittsburgh, PA, USA
* To whom correspondence should be addressed. E-mail: gla6{at}pitt.edu.
Neural-epithelial interactions are hypothesized to play an important role in bladder function. We determined whether spinal cord injury (SCI) altered several indicators of urinary bladder epithelium barrier function including continuity of the surface umbrella cell layer, transepithelial resistance (TER), and urea and water permeability. Within 2 h of SCI significant changes in urothelium were noted including disruption of the surface umbrella cells and an ~ 50 % decrease in TER. By 24 h TER reached a minimum and was accompanied by significant increases in water and urea permeability. Regeneration of the surface urothelium was accomplished by 14 d following SCI and this was accompanied by a return to normal TER and urea and water permeabilities. This early disruption of the uroepithelial permeability and accompanying changes in urothelial morphology were prevented by pretreatment with hexamethonium (a blocker of ganglion transmission) indicating the involvement of sympathetic or parasympathetic input to the urinary bladder. In addition, prior treatment with capsaicin worsened the effect of SCI on urothelial permeability suggesting that capsaicin-sensitive afferents may play a protective role in the process. These results demonstrate that SCI results in a significant disruption of the urinary bladder urothelium, and that these changes may be mediated in part by an interaction with bladder nerves.
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