TY - JOUR
T1 - Enhanced Adenosine Triphosphate Release From the Urothelium of Patients With Painful Bladder Syndrome
T2 - A Possible Pathophysiological Explanation
AU - Kumar, Vivek
AU - Chapple, Christopher R.
AU - Surprenant, Ann Marie
AU - Chess-Williams, Russell
PY - 2007/10
Y1 - 2007/10
N2 - Purpose: We established the level of adenosine triphosphate release by the urothelium in patients with painful bladder syndrome and compared it with that from the normal human bladder. Materials and Methods: Biopsies of urothelium from patients with painful bladder syndrome were subjected to stretch by 130% and 150% of the original length, and 10 Hz electric stimulation. A luciferase assay was used to quantify adenosine triphosphate release. The neurotoxin tetrodotoxin was used to block the neuronal source of adenosine triphosphate release. Results: There was a significantly greater release of adenosine triphosphate following mechanical stretch of the urothelium from painful vs control bladders. The increase in adenosine triphosphate release in painful vs control bladders was statistically significant whether expressed in absolute values (mean ± SE 3,791.4 ± 667.9 vs 77.6 ± 16.2 pM gm-1 tissue) or as an increase over baseline (282.2% ± 24.8% vs 175.4% ± 21.7%). Similarly there was a significant release of adenosine triphosphate following electrical field stimulation of the urothelium from painful vs control bladders (1,348.6 ± 278.2 vs 61.7 ± 10.1 pM gm-1 tissue, p <0.005), representing a 278% ± 41.5% vs 137.9% ± 4.4% increase above baseline (p <0.005). The source of adenosine triphosphate release was nonneuronal in 89% of painful bladders and in 84% of control bladders. Conclusions: There is a significantly increased level of adenosine triphosphate release from the urothelium of painful bladders in comparison to that from normal bladders, suggesting an important potential functional role for adenosine triphosphate in this condition.
AB - Purpose: We established the level of adenosine triphosphate release by the urothelium in patients with painful bladder syndrome and compared it with that from the normal human bladder. Materials and Methods: Biopsies of urothelium from patients with painful bladder syndrome were subjected to stretch by 130% and 150% of the original length, and 10 Hz electric stimulation. A luciferase assay was used to quantify adenosine triphosphate release. The neurotoxin tetrodotoxin was used to block the neuronal source of adenosine triphosphate release. Results: There was a significantly greater release of adenosine triphosphate following mechanical stretch of the urothelium from painful vs control bladders. The increase in adenosine triphosphate release in painful vs control bladders was statistically significant whether expressed in absolute values (mean ± SE 3,791.4 ± 667.9 vs 77.6 ± 16.2 pM gm-1 tissue) or as an increase over baseline (282.2% ± 24.8% vs 175.4% ± 21.7%). Similarly there was a significant release of adenosine triphosphate following electrical field stimulation of the urothelium from painful vs control bladders (1,348.6 ± 278.2 vs 61.7 ± 10.1 pM gm-1 tissue, p <0.005), representing a 278% ± 41.5% vs 137.9% ± 4.4% increase above baseline (p <0.005). The source of adenosine triphosphate release was nonneuronal in 89% of painful bladders and in 84% of control bladders. Conclusions: There is a significantly increased level of adenosine triphosphate release from the urothelium of painful bladders in comparison to that from normal bladders, suggesting an important potential functional role for adenosine triphosphate in this condition.
UR - http://www.scopus.com/inward/record.url?scp=34548410930&partnerID=8YFLogxK
U2 - 10.1016/j.juro.2007.05.116
DO - 10.1016/j.juro.2007.05.116
M3 - Article
C2 - 17707056
AN - SCOPUS:34548410930
SN - 0022-5347
VL - 178
SP - 1533
EP - 1536
JO - Journal of Urology
JF - Journal of Urology
IS - 4
ER -