Angiotensin II in child urinary bladder: functional and autoradiographic studies

Lam, D.S.H.; Dias, Leonora S.; Moore, Kate H.; Burcher, Elizabeth

doi:10.1046/j.1464-410x.2000.00771.x

Cited by 17 publications

(18 citation statements)

References 21 publications

(34 reference statements)

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“…Tanabe et al [39]found AT1 rather than AT2 to predominantly mediate ANG II-induced contraction in the rat urinary bladder, and Lam et al [40]demonstrated the presence of functional AT1 as opposed to AT2 in child detrusor smooth muscle. Persson et al [41]also concluded that the effect of ANG II on bladder smooth muscle tone was minor and that it was mediated by stimulation of the AT1 subtype receptor.…”

Section: Discussionmentioning

confidence: 99%

Genetic Polymorphism of the Renin-Angiotensin System on the Development of Primary Vesicoureteral Reflux

Yim

Jung²,

Choi³

et al. 2004

Am J Nephrol

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Background: The familial clustering of vesicoureteral reflux (VUR) has suggested a genetic basis. This study was designed to investigate the genetic polymorphism of the renin-angiotensin system (RAS) in Korean children. Methods: Genetic polymorphism of angiotensin-converting enzyme (ACE) and angiotensin II receptor genes was evaluated in 67 primary VUR patients and compared to 58 controls with no urological abnormalities. To detect the relation of the risk factors of primary VUR with the genetic polymorphism, the distribution of ACE, AT1 and AT2 genotypes after stratification by risk factors was also studied in the primary VUR patients. Results: The incidence of AT2 A-1332G transition was significantly lower in primary VUR patients (p = 0.047). Furthermore, in the case of combination of ACE and AT2 gene, a significantly lower incidence of primary VUR was seen with II genotype of ACE and A-1332G transition in the AT2 receptor gene (p = 0.003). Concerning the risk factors of primary VUR, there were no biologically significant results. Conclusions: These findings indicate that a lower incidence of AT2 A-1332G transition is seen in primary VUR patients, at least in the Korean population. Also, in the case of combination of ACE and AT2 gene, the combination of ACE II genotype and AT2 A-1332G transition occurs infrequently in primary VUR.

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Section: Discussionmentioning

confidence: 99%

Genetic Polymorphism of the Renin-Angiotensin System on the Development of Primary Vesicoureteral Reflux

Yim

Jung²,

Choi³

et al. 2004

Am J Nephrol

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“…An autocrine/paracrine reninangiotensin system has been identified in the urinary bladder (Weaver-Osterholtz et al, 1996), and angiotensin II (ATII) formation was demonstrated in human isolated detrusor smooth muscle Lindberg et al, 1994;Waldeck et al, 1997). ATII receptors have been demonstrated by different methods in animal as well as human detrusor (Anderson et al, 1984;Lam et al, 2000). ATII was reported to contract the urinary bladder of several species, but with a wide range of relative potencies (Erspamer et al, 1973;Anderson et al, 1984).…”

Section: Peripheral Targetsmentioning

confidence: 99%

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Andersson

Wein²

2004

Pharmacol Rev

453

364

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“…The current data showed the reduction of AT1 expression caused by P-BOO visually and temporally using immunohistochemical staining. Several investigators have shown that Ang II causes pronounced contraction of bladder smooth muscles in some species, including humans [7,8,9,10,11], and the effect is mediated by the AT1. The downregulation of AT1 in outlet-obstructed rat was observed by Saito et al [12] who showed significantly weaker contractility of human detrusor muscle by Ang II in neurogenic bladders than controls.…”

Section: Discussionmentioning

confidence: 99%

Changes in Angiotensin II Type 1 Receptor Expression in the Rat Bladder by Bladder Outlet Obstruction

et al. 2012

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Purpose: To demonstrate the change in the expression of angiotensin II type 1 receptor (AT1) in the rat bladder with partial bladder outlet obstruction (P-BOO). Materials and Methods: Bladder specimens were obtained from 12-week-old Wistar female rats that were divided into two groups, a P-BOO group and a control group. The rats of the P-BOO group were divided into six groups: a sham-operated control group, 1 day postoperatively, 2 days postoperatively, 4 days postoperatively, 7 days postoperatively and 14 days postoperatively. The cystometric findings and immunohistochemical staining of the detrusor muscle with the AT1 antibody were compared in each group. Results: AT1 localized on the cell membrane of the detrusor smooth muscle and in cytoplasm of suburothelial myofibroblasts in the control rats. The expression of AT1 disappeared in the detrusor muscle and suburothelial myofibroblasts in P-BOO, but AT1 was highly expressed in urothelial cells 1 day after surgery. The expression of AT1 in urothelial cells gradually decreased with time after surgery. AT1 completely disappeared in urothelial cells 14 days after surgery. Conclusions: The present study demonstrated that the site of AT1 expression changes in response to the mechanical stress caused by P-BOO, and finally there was no expression of AT1 in rat bladder tissue following P-BOO. These data suggest the change in AT1 expression may play a role in bladder function.

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Angiotensin II in child urinary bladder: functional and autoradiographic studies

Cited by 17 publications

References 21 publications

Genetic Polymorphism of the Renin-Angiotensin System on the Development of Primary Vesicoureteral Reflux

Genetic Polymorphism of the Renin-Angiotensin System on the Development of Primary Vesicoureteral Reflux

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Changes in Angiotensin II Type 1 Receptor Expression in the Rat Bladder by Bladder Outlet Obstruction

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