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Am J Physiol Renal Physiol 284: F966-F976, 2003. First published January 14, 2003; doi:10.1152/ajprenal.00359.2002
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Vol. 284, Issue 5, F966-F976, May 2003

Disruption of bladder epithelium barrier function after spinal cord injury

Gerard Apodaca1, Susanna Kiss2, Wily Ruiz2, Susan Meyers2, Mark Zeidel1, and Lori Birder2,3

1 Laboratory of Epithelial Cell Biology, Department of Cell Biology and Physiology, 2 Renal-Electrolyte Division, Department of Medicine, and 3 Department of Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261

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 uroepithelium 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 uroepithelium was accomplished by 14 days after SCI and was accompanied by a return to normal TER and urea and water permeabilities. This early disruption of the uroepithelial permeability and accompanying changes in uroepithelial morphology were prevented by pretreatment with hexamethonium (a blocker of ganglion transmission), indicating involvement of sympathetic or parasympathetic input to the urinary bladder. In addition, prior treatment with capsaicin worsened the effect of SCI on uroepithelial 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 uroepithelium and that these changes may be mediated in part by an interaction with bladder nerves.

uroepithelium; urea and water permeability; bladder nerves


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