The Functional Effects of Long-Term Outlet Obstruction on the Rabbit Urinary Bladder

Kato, Kumiko; Monson, Frederick C.; Longhurst, Penelope A.; Wein, Alan J.; Haugaard, Niels; Levin, Robert M.

doi:10.1016/s0022-5347(17)40038-3

Cited by 164 publications

(104 citation statements)

References 20 publications

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“…On the other hand, inhibition of angiogenesis by L-NAME administration would make ischemic damage and bladder contractile dysfunction worse, which is also reflected in the marked augmentation of bladder weight at 8-wk obstruction. Since bladder weight has been demonstrated to be an excellent indicator of the severity of obstructive dysfunctions (14,25), we believe that this confirms the protective effect of L-arginine. Denervation in the obstructed bladders was estimated by means of neurofilament staining and a ChAT functional assay. It is the small nerve tracts that innervate the bladder smooth muscle tissues.…”

Section: Discussionsupporting

confidence: 69%

“…Consistent with our results of contractile properties and bladder weight in 2 and 8 wk PBOO, CS activity marked a difference only at the 8-wk treated L-arginine group compared with non-treatment group. Because PBOO of the rabbit induces a shift from aerobic to anaerobic metabolism, dysfunction of the bladder correlates with the decreased cellular concentration of high-energy phosphates generated through oxidative metabolism (14,15). The cellular mechanism responsible for decreased oxidative metabolism involves decreased mitochondrial enzyme activity, such as decreases in the activity of CS (12).…”

Section: Discussionmentioning

confidence: 99%

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Effects ofl-arginine andl-NAME on chronic partial bladder outlet obstruction in rabbit

Lin

Levin²,

Chichester³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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(NO) is synthesized from L-arginine by nitric oxide synthase (NOS). NOS can be inhibited by N G -nitro-L-arginine methyl ester (L-NAME) and stimulated by supplementing the diet with L-arginine. The aim of this study was to investigate the influence of NOS activity on the response of rabbits to chronic partial bladder outlet obstruction (PBOO). Surgical PBOOs (2 and 8 wk) were performed on male New Zealand White rabbits. Before obstruction, one-third of the animals were premedicated for 7 days with L-NAME and another third with L-arginine. The results are summarized as follows. First, bladder weight after 8-wk PBOO was significantly lower in animals treated with L-arginine compared with both untreated and rabbits treated with L-NAME. Second, contractile function decreased progressively with PBOO duration. However, after 8 wk of PBOO, the L-arginine group had significantly greater contractile function compared with the notreatment group, and the L-NAME group had significantly lower contractile function compared with the no-treatment group. Third, at 8 wk following PBOO, the level of protein oxidation and nitration was lowest for the L-arginine group and highest in the L-NAME group. These studies clearly demonstrated that increasing blood flow by stimulating NOS significantly protected the bladder from PBOO dysfunctions, whereas inhibiting blood flow by L-NAME enhanced the dysfunctions mediated by PBOO. contractility; angiogenesis; nitric oxide NITRIC OXIDE (NO), a neurotransmitter responsible for relaxation activity in the lower urinary tract and corpus cavernosum, is synthesized from L-arginine in a reaction catalyzed by NO synthase (NOS) (6). NO is also known to be a powerful and ubiquitous regulator of vascular tone, and thus in several systems is shown to regulate blood flow. In cardiac studies, impaired release of NO may be an important factor in the development of ischemia-reperfusion (I/R) injury. Conversely, it has been demonstrated that administration of NO donors or L-arginine reduces infarct size and improves the postischemic recovery of cardiac performance and endothelial function in animal models of myocardial ischemia and reperfusion (28,36,37). Similarly, other studies have shown that exogenously administered L-arginine decreases oxidative stress in the liver and brain (9) and that an increase in NO formation has a beneficial effect on the progression of cellular and molecular parameters of tubulointerstitial fibrosis caused by obstruction of the ureter (27). With regards to bladder function, our previous study demonstrated that feeding rabbits a diet high in L-arginine was beneficial for both control rabbits and those with 2 wk of severe partial bladder outlet obstruction (PBOO) (38).Contradicting the protective effects, NO is reported to generate free radicals in I/R injury, which has been shown in other studies to be one of the primary causes of progression of bladder dysfunction (3). It has been demonstrated that NO-related damage due to nitrotyrosine was elevated with PBOO (23). Pretreatment wi...

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Section: Discussionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Effects ofl-arginine andl-NAME on chronic partial bladder outlet obstruction in rabbit

Lin

Levin²,

Chichester³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

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“…BOO is divided into three stages: 1) hypertrophy, 2) compensation and 3) decompensation (2). Bladders in the first hypertrophic stage show increased contractile force (9,25,37). bFGF is also upregulated during hypertrophy but decreases to normal levels during decompensation (4,9).…”

Section: Discussionmentioning

confidence: 99%

Basic fibroblast growth factor modulates proliferation and collagen expression in urinary bladder smooth muscle cells

Imamura¹,

Kanematsu²,

Yamamoto³

et al. 2007

American Journal of Physiology-Renal Physiology

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Bladder hypertrophy is a general consequence of bladder outlet obstruction (BOO) and a typical phenomenon observed in clinical urologic diseases such as benign prostatic hyperplasia and neurogenic bladder. It is characterized by smooth muscle hyperplasia, altered extracellular matrix composition, and increased contractile function. Various growth factors are likely involved in hypertrophic pathophysiology, but their functions remain unknown. In this report, the role of basic fibroblast growth factor (bFGF) was investigated using a rat bladder smooth muscle cell (BSMC) culture system and an original animal model, in which bFGF was released from a gelatin hydrogel directly onto rat bladders. bFGF treatment promoted BSMC proliferation both in vitro and in vivo. In vitro, bFGF downregulated the expression of type I collagen, but upregulated type III collagen. ERK1/2, but not p38MAPK, was activated by bFGF, whereas inhibition of ERK1/2 by PD98059 reversed bFGF-induced BSMC proliferation, type I collagen downregulation, and type III collagen upregulation. In the in vivo release model, bFGF upregulated type III collagen and increased the contractile force of treated bladders. In parallel with these findings, hypertrophied rat bladders created by urethral constriction showed increased urothelial bFGF expression, BSMC proliferation, and increased type III collagen expression compared with sham-operated rats. These data suggest that bFGF from the urothelium could act as a paracrine signal that stimulates the proliferation and matrix production of BSMC, thereby contributing to the hypertrophic remodeling of the smooth muscle layer.

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“…In previous studies on bladder obstructions in rabbits, it is clear that the greater the increase in bladder mass following obstruction, the more severe the contractile and structural dysfunctions [23,24] . Alternately, the lower the increase in bladder mass, the less severe the dysfunction [23,24] .…”

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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The Functional Effects of Long-Term Outlet Obstruction on the Rabbit Urinary Bladder

Cited by 164 publications

References 20 publications

Effects ofl-arginine andl-NAME on chronic partial bladder outlet obstruction in rabbit

Effects ofl-arginine andl-NAME on chronic partial bladder outlet obstruction in rabbit

Basic fibroblast growth factor modulates proliferation and collagen expression in urinary bladder smooth muscle cells

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

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