Role of the urothelium in urinary bladder dysfunction following spinal cord injury.

A consequence of spinal cord injury is a change in bladder reflex pathways resulting in the emergence of detrusor hyperreflexia and increased activity of the urethral sphincter. A basis for some of these alterations could be changes in the environment of bladder sensory nerve endings at the target organ. Recent evidence suggests that the urothelium (the lining of the urinary bladder) plays a prominent role in modulating bladder sensory nerve ending excitability. It is conceivable that factors and processes affecting the plasticity of bladder neurons after spinal cord injury may be partly due to changes occurring in the urothelium. Although the urothelium has classically been thought of as a passive barrier to ions/solutes, a number of novel properties have been recently attributed to these cells. Our work and that of others clearly demonstrates that the urothelium exhibits both "sensor" (expression of sensor molecules or response to thermal, mechanical and chemical stimuli) as well as "transducer" (release of factors/transmitters) properties. Taken together, these and other findings discussed in this chapter suggest a sensory function for the urothelium and that alterations in urothelial properties may contribute to afferent abnormalities following spinal cord injury.