UroToday - There are currently two well-known bladder hypersensory syndromes - overactive bladder (OAB) and interstitial cystitis (BPS/IC). Because BPS/IC is associated with chronic bladder pain, it represents potentially a more challenging clinical problem. There are no treatments that target specifically the bladder sensory pathways.

Recent data suggest that bladder urothelial cells do more than provide a barrier function, but also may initiate bladder sensory signals. They can release putative neurotransmitters including ATP and nitric oxide in response to stretch or pharmacologic stimuli. They also express receptors typically found on neurons. Skin epithelial cells can function as sensors, and it may be that bladder urothelial cells function this way as well.

To better understand the potential for the bladder urothelial cell to participate in bladder sensory signaling, Yan Sun and colleagues from the University of Maryland designed single cell electrophysiological experiments in human normal and BPS/IC bladder urothelial cells. An inward rectifying potassium current was detected in all cells. A decreased conductance was detected in BPS/IC bladder urothelial cells. Conversely, increased potassium conductivity was induced in BPS/IC bladder urothelial cells by exposure to heparin binding epidermal growth factor-like growth factor (HB-EGF). The electrophysiological phenotype of normal and BPS/IC bladder urothelial cells was switched by exposing them to epidermal growth factor and genistein as well as HB-EGF.

The authors believe their findings suggest that potassium currents caused by alterations in growth factor levels could play a role in the pathophysiology of bladder urothelial cells in BPS/IC patients, yielding a potential future target for therapeutic intervention.

By Philip Hanno, MD, MPH

Am J Physiol Cell Physiol (July 12, 2006).
Link Here.

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