PURPOSE: Recent studies revealed that interstitial cells (ICs) are widely distributed in genitourinary tract, and suggested their involvement in spontaneous electrical activity and muscle contraction. However, nitric oxide (NO) is thought to play a ro...
PURPOSE: Recent studies revealed that interstitial cells (ICs) are widely distributed in genitourinary tract, and suggested their involvement in spontaneous electrical activity and muscle contraction. However, nitric oxide (NO) is thought to play a role in bladder overactivity related with BOO. The purposes of this study were to investigate the effect of detrusor overactivity induced by BOO on ICs and nitric oxide synthase (NOS) isoforms in rat urinary bladder
MATERIALS AND METHODS: Female Sprague-Dawley rats (230-240 g, n=60) were divided into 2 groups: control (group Con, n=30), partial bladder outlet obstruction (group BOO, n=30). The BOO group underwent partial bladder outlet obstruction. After 4 weeks, the urodynamic study measuring contraction interval and contraction pressure was done. The expression and cellular localization of ICs, endothelial nitric oxide synthase (eNOS) and neuronal NOS (nNOS) were determined by Western blot and immunohistochemistry in rat urinary bladder.
RESULTS: Four weeks after surgery, filling cystometry demonstrated a reduced interval between voiding contractions and an increased voiding pressure in BOO bladders. Estimated contraction interval (min, mean ± SE) significantly decreased in BOO group (2.9±0.35) compared with Con group (6.1±0.05)(p<0.05). In BOO bladders, the thickness of suburothelial, and detrusor smooth muscle layers were increased. Population of Kit positive ICs was increased in both of suburothelial and muscle layers in BOO bladders. ICs had a close contact with each other and neighboring nNOS expressing cells.
CONCLUSIONS: These results demonstrated the increased population of ICs in the BOO rat model, and suggest that the functional change of ICs and NOS isoforms may contribute to the pathophysiology of bladder overactivity induced by BOO.