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Effect of detrusor overactivity on the expression of aquaporins and nitric oxide synthase in rat urinary bladder following bladder outlet obstruction.

Authors: Kim, SO  Choi, D  Song, SH  Ahn, KY  Kwon, D  Park, K  Ryu, SB 
Citation: Kim SO, etal., Can Urol Assoc J. 2013 May-Jun;7(5-6):E268-74. doi: 10.5489/cuaj.993.
Pubmed: (View Article at PubMed) PMID:23766828
DOI: Full-text: DOI:10.5489/cuaj.993

BACKGROUND: Aquaporins (AQPs) have recently been reported to be expressed in rat and human urothelium. Nitric oxide (NO) is thought to play a role in the bladder overactivity related to bladder outlet obstruction (BOO). The purpose of this study is to investigate the effect of BOO on the expression of AQP2-3 and nitric oxide synthase (NOS) isoforms in rat urothelium. METHODS: Female Sprague-Dawley rats (230-240 g, n = 60) were divided into 2 groups. The control group (n = 30) and the partial bladder outlet obstruction (BOO) group (n = 30). After 4 weeks, we performed a urodynamic study to measure the contraction interval and contraction pressure. The expression and cellular localization of AQP2-3, endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) were determined by Western blot and immunohistochemistry. RESULTS: On the cystometrogram, the estimated contraction interval time (minutes, mean +/- SE) was significantly lower in the BOO group (3.0 +/- 0.9) than in the control group (6.3 +/- 0.4; p < 0.05). AQP2 was localized in the cytoplasm of the epithelium, whereas AQP3 was found only in the cell membrane of the epithelium. The protein expression of AQP2-3, eNOS and nNOS was significantly increased in the BOO group. CONCLUSION: Detrusor overactivity induced by BOO causes a significant increase in the expression of AQP2-3, eNOS, and nNOS in rat urinary bladder. This may imply that the AQPs and NOS isoforms have a functional role in the bladder dysfunction that occurs in association with BOO.


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CRRD Object Information
CRRD ID: 7257604
Created: 2013-08-27
Species: All species
Last Modified: 2013-08-27
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.