Overexpression of epithelial sodium channels in epithelium of human urinary bladder with outlet obstruction

Araki, Isao; Du, Shanshan; Kamiyama, Manabu; Mikami, Yuki; Matsushita, Kazumichi; Komuro, Mitsuo; Furuya, Yasuhisa; Takeda, Masayuki

doi:10.1016/j.urology.2004.06.064

Cited by 58 publications

(48 citation statements)

References 20 publications

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“…18 This possibility may be further supported by the results of Araki and colleagues. 25 They studied the role of the ENaC in bladder dysfunction in male patients who were diagnosed clinically with BOO. They reported that the expression levels of ENaC were significantly greater in patients with BOO than in controls and correlated with the patients' storage symptom scores.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…A dramatic example of net water or solute movement is in hibernating bears, which are capable of reabsorbing their entire daily urine production during the months of winter [13]. Furthermore, Araki et al [14] tried to investigate the role of the epithelial sodium channel (ENaC) in bladder overactivity in patients who were diagnosed clinically with bladder outlet obstruction. They showed that ENaC expression correlated significantly with the patients' storage symptom score, and the expression levels of ENaC in patients with bladder outlet obstruction were significantly greater than those of controls.…”

Section: Discussionmentioning

confidence: 99%

The Expression of AQP1 and eNOS in Menopausal Rat Urinary Bladder

et al. 2010

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Purpose: Aquaporins (AQPs) have been reported to be expressed in rat and human urothelium. Nitric oxide (NO) is thought to play an important role in the bladder overactivity related to menopause. The purpose of this study was to investigate the effect of hormonal alteration on the expression of AQP1 and eNOS in menopausal rat urinary bladder. Materials and Methods: Female Sprague-Dawley rats (230-240 g, N=30) were divided into three groups: control (N=10), bilateral ovariectomy (Ovx, N=10), and bilateral ovariectomy followed by subcutaneous injections of 17β -estradiol (50 mg/kg/day, Ovx+Est, N=10). After 4 weeks, urodynamic studies measuring the contraction interval and contraction pressure were done. The expression and cellular localization of AQP1 and eNOS were determined by performing Western blotting and immunohistochemistry on the rat urinary bladder. Results: The approximate contraction interval (min) was significantly decreased in the Ovx group (3.9±0.25) compared to the control group (6.7±0.15), and was increased after estrogen treatment (9.7±0.22) (p<0.05). The AQP1 and eNOS immunoreactivities were localized in the same areas: capillaries, arterioles, and venules of the lamina propria. The protein expression of AQP1 was not changed significantly, whereas eNOS expression was significantly decreased in the Ovx group and restored to the control value in the Ovx+Est group. Conclusions: This study showed that ovariectomy causes a significant change in e-NOS expression without a change in AQP1 in menopausal rat urinary bladder. This may imply that e-NOS has a functional role in the bladder overactivity that occurs in association with menopause.

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“…Interestingly, a mechanosensitive role for ENaC has also been proposed in the urinary bladder, where the release of ATP from epithelial cells in response to increased hydrostatic pressure was prevented by amiloride (285). Furthermore, ENaC expression was found to be increased in the bladder mucosa patients with urinary outlet obstruction (13). Expression of ␤ENaC also seems to be critical to the autoregulation of renal blood flow, as myogenic constriction was compromised in a murine model poorly expressing this subunit (105,154).…”

Section: Other Roles For Enac In Vascular-cardio-renal Diseasementioning

confidence: 99%

ENaCs and ASICs as therapeutic targets

Qadri

Rooj

Fuller

2012

American Journal of Physiology-Cell Physiology

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The epithelial Na+channel (ENaC) and acid-sensitive ion channel (ASIC) branches of the ENaC/degenerin superfamily of cation channels have drawn increasing attention as potential therapeutic targets in a variety of diseases and conditions. Originally thought to be solely expressed in fluid absorptive epithelia and in neurons, it has become apparent that members of this family exhibit nearly ubiquitous expression. Therapeutic opportunities range from hypertension, due to the role of ENaC in maintaining whole body salt and water homeostasis, to anxiety disorders and pain associated with ASIC activity. As a physiologist intrigued by the fundamental mechanics of salt and water transport, it was natural that Dale Benos, to whom this series of reviews is dedicated, should have been at the forefront of research into the amiloride-sensitive sodium channel. The cloning of ENaC and subsequently the ASIC channels has revealed a far wider role for this channel family than was previously imagined. In this review, we will discuss the known and potential roles of ENaC and ASIC subunits in the wide variety of pathologies in which these channels have been implicated. Some of these, such as the role of ENaC in Liddle's syndrome are well established, others less so; however, all are related in that the fundamental defect is due to inappropriate channel activity.

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Overexpression of epithelial sodium channels in epithelium of human urinary bladder with outlet obstruction

Cited by 58 publications

References 20 publications

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

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

The Expression of AQP1 and eNOS in Menopausal Rat Urinary Bladder

ENaCs and ASICs as therapeutic targets

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