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

Abstract

E268research research AbstractBackground: 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.

Persistent storage symptoms after TURP can be predicted with a nomogram derived from the ice water test

“…Furthermore, changes in the detrusor muscle innervation and muscle structure have been found. Recently also potassium channels decrease, ischemic‐induced changes and the nitric oxide pathway changes were found . Barbosa et al compared bladder histology between patients undergoing TURP vs non‐obstructed control patients and found upregulations of collagen types I and III.…”

Loss of Caveolin 1 is Associated With the Expression of Aquaporin 1 and Bladder Dysfunction in Mice

“…In our previous report, detrusor overactivity caused by BOO led to a significant increase in the expression of AQP2–3, and nitric oxide synthase (endothelial nitric oxide synthase, neuronal nitric oxide synthase) in rat urinary bladder. In the study, we suggested that the AQPs and nitric oxide synthase isoforms might have a specific role in bladder dysfunction that is related with bladder change following BOO [ 12 ].…”

“…In our previous reports, we demonstrated altered expression of AQP1 in the urinary bladder of rats presenting detrusor overactivity [ 12 - 14 ]. Further, in a more recent study, we speculated about the relation between AQP1 and CAV1 in the urinary bladder, and found that they are significantly overexpressed upon detrusor overactivity (caused by bladder outlet obstruction [BOO]).…”

“…Further, in a more recent study, we speculated about the relation between AQP1 and CAV1 in the urinary bladder, and found that they are significantly overexpressed upon detrusor overactivity (caused by bladder outlet obstruction [BOO]). Moreover, AQP1 and CAV1 were found to colocalize in the suburothelial microvasculature [ 12 - 14 ]. Based on earlier observations, we suggested that AQP1 and CAV1 might be closely associated with bladder signal activity that may, in turn indicate their role in detrusor overactivity.…”

Is benign prostatic obstruction surgery indicated for improving overactive bladder symptoms in men with lower urinary tract symptoms?

“…By finding no significance after addition of vardenafil, the authors postulated that increase of guanylate cyclase was the main target for nitric oxide/cyclic guanosine monophosphate pathway. In another study using the same experimental model, Kim et al [31] have shown a significant increase of endothelial nitric oxide synthase and neuronal nitric oxide synthase in rats with induced bladder outlet obstruction. The same authors reported an increase of the expression of aquaporin2-3, which is also involved in the nitric oxide pathway.…”