Nitric oxide in the lower urinary tract: physiological and pathological implications

Mumtaz, Faiz; Ma, Ketao; Thompson, CS; Morgan, RJ; Mikhailidis, DP

doi:10.1046/j.1464-410x.2000.00459.x

Cited by 46 publications

(34 citation statements)

References 118 publications

(160 reference statements)

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“…In the rat, mouse, and rabbit there are studies indicating the notable effects of L -arginine and NOS inhibitors on the bladder response to PBOO and ischemia reperfusion [18][19][20][21][22] . In the rat and mouse, the NOS inhibitor aminoguanidine causes an amelioration of functional and fibrotic changes in the bladder after PBOO [20] .…”

Section: Discussionmentioning

confidence: 99%

Role of Nitric Oxide in Urinary Bladder Function: Effect of <i>L</i>-Arginine

Whitbeck

Chichester²,

Sokol³

et al. 2007

Urol Int

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Background: Evidence indicates that decreased blood flow to the bladder plays a major role in obstructive bladder dysfunction in the rabbit model of partial bladder outlet obstruction (PBOO), and that nitric oxide (NO) regulation of blood flow may be important in modulating the degree of obstructive bladder dysfunction. The specific aim of our study is to determine the effect of feeding rabbits a diet high in L-arginine on the response to PBOO. Materials and Methods: Sixteen male NZ White rabbits were separated into 4 groups of 4 each. The rabbits in groups 1 and 3 underwent PBOO. The rabbits in groups 2 and 4 were sham-operated. For 1 week prior to surgery, and 2 weeks postoperatively, each rabbit in groups 1 and 2 was put on a diet containing 7% arginine. Rabbits in groups 3 and 4 were on a normal diet (0.76% arginine). Results: PBOO resulted in a greater increase in bladder weight in the control group than the arginine group. PBOO resulted in a greater decrease in compliance in the control group than the arginine group. The contractile responses to all agents in the arginine control group were greater than in the control normal diet group. PBOO resulted in a greater decrease in the response to field stimulation in the control group than in the arginine group. Conclusions: These studies clearly demonstrate that feeding rabbits a diet high in L-arginine was beneficial for the control rabbits, and reduced the level of dysfunctions following PBOO.

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Section: Discussionmentioning

confidence: 99%

Role of Nitric Oxide in Urinary Bladder Function: Effect of <i>L</i>-Arginine

Whitbeck

Chichester²,

Sokol³

et al. 2007

Urol Int

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“…Also, NO is thought to play a role in bladder overactivity, which may be associated with impairment in the NO signaling pathway. 16,17 On the basis of these findings, we hypothesized that the AQPs and NOS might be involved in the physiology of bladder dysfunction induced by BOO. The purpose of this study was to investigate the impact of BOO on the expression of the AQP2-3 and NOS isoforms in rat urinary bladder.…”

Section: Introductionmentioning

confidence: 99%

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

Kim

Choi

Song

et al. 2013

CUAJ

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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.

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“…eNOS affects blood vessels, and nNOS affects nerve fibers. All three isoforms have been identified in the lower urinary tract of humans [30]. NO is generated from the guanidino nitrogen of L -arginine by NOS.…”

Section: Discussionmentioning

confidence: 99%

“…Mumtaz et al [30] showed that systemic infusion of NO donors increases urethral relaxation and decreases baseline urethral pressure. Andersson et al [19] reported that electrically induced relaxation of rabbit urethra strips was significantly reduced after pretreatment with NOS inhibitors in an in vitro study.…”

Section: Discussionmentioning

confidence: 99%

The Relaxant Effect of Ginseng Saponin on the Bladder and Prostatic Urethra: An in vitro and in vivo Study

Jang

Cho²,

Kang³

et al. 2012

Urol Int

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Aim: To assess the effects of ginseng saponin on relaxation of the bladder and prostatic urethra and to determine its mechanism of action. Materials and Methods: For the in vitro study, prostatic urethra muscle strips were harvested from 18 male New Zealand rabbits. The strips were mounted in organ baths and connected to force displacement transducers. After stabilization, maximal tissue contractions were obtained by the application of phenylepinephrine to the urethra strips, and a dose-response curve for ginseng saponin was constructed (10^–6–10^–2M). After pretreatment of urethra strips with N-nitro-L-arginine methyl ester (L-NAME), another dose-response curve for ginseng saponin was constructed. For the in vivo study, we used adult male Sprague-Dawley rats divided into three groups [control, partial bladder outlet obstruction (PBOO) and saponin-fed groups], and we monitored the vesical pressure (P_ves) and urethral perfusion pressure (UPP). Results: The ginseng saponin induced a significant dose-dependent relaxant effect on the prostatic urethra strips. A significant relaxant effect of ginseng saponin was observed from 10^–3M, and ginseng saponin significantly relaxed urethra strips by 50.2 ± 20.26% at 10^–2M. The relaxant effect was partially inhibited with L-NAME pretreatment. In the in vivo study, the change in UPP between baseline and relaxation was significantly higher in the saponin group than in the control or PBOO group (p < 0.001). The saponin group showed a significantly lower baseline P_ves than the PBOO group. Conclusions: We observed a significant relaxation effect of ginseng saponin on the bladder and prostatic urethra in both in vitro and in vivo studies. The mechanism by which ginseng saponin induces relaxation appears to involve the nitric oxide/nitric oxide synthase pathway.

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Nitric oxide in the lower urinary tract: physiological and pathological implications

Cited by 46 publications

References 118 publications

Role of Nitric Oxide in Urinary Bladder Function: Effect of <i>L</i>-Arginine

Role of Nitric Oxide in Urinary Bladder Function: Effect of <i>L</i>-Arginine

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

The Relaxant Effect of Ginseng Saponin on the Bladder and Prostatic Urethra: An in vitro and in vivo Study

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