Development of Idiopathic Detrusor Underactivity in Women: From Isolated Decrease in Contraction Velocity to Obvious Impairment of Voiding Function

Cucchi, A.; Quaglini, Silvana; Rovereto, B.

doi:10.1016/j.urology.2007.11.145

Cited by 37 publications

(27 citation statements)

References 12 publications

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“…Although perhaps less clinically relevant than OAB, detrusor overactivity, or bladder hyperreflexia, detrusor underactivity is a clinical problem that is seen most often in men, although women are also affected (16,17). It consists of reduced muscle contraction, strength, or velocity and often results in incomplete voiding, postvoid residual, prolonged emptying, and reduced free uroflow (16,17). Detrusor underactivity can be neurogenic, idiopathic, or a result of bladder outflow obstruction (16,17 …”

Section: Discussionmentioning

confidence: 99%

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Role of p75^NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

Klinger

Vizzard²

2008

American Journal of Physiology-Renal Physiology

106

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NTR in bladder function in control and CYP-treated rats was determined using conscious cystometry and immunoneutralization or PD90780, a compound known to specifically block NGF binding to p75NTR . An anti-p75 NTR monoclonal antibody or PD90780 was infused intravesically and cystometric parameters were evaluated. Both methods of p75 NTR blockade significantly (P Յ 0.05) decreased the intercontraction interval and void volume in control and CYP-treated rats. Intravesical infusion of PD90780 also significantly (P Յ 0.001) increased intravesical pressure and increased the number of nonvoiding contractions during the filling phase. Control intravesical infusions of isotype-matched IgG and vehicle were without effect. Intravesical instillation of PD90780 significantly (P Յ 0.01) reduced the volume threshold to elicit a micturition contraction in control rats (no inflammation) and CYP-treated in a closed urinary bladder system. These studies demonstrate 1) ubiquitous p75 NTR expression in urinary bladder and increased expression with CYP-induced cystitis and 2) p75 NTR blockade at the level of the urinary bladder produces bladder hyperreflexia in control and CYP-treated rats. The overall activity of the urinary bladder reflects the balance of NGF-p75 NTR and NGF-TrkA signaling. NTR belongs to the tumor necrosis factor-␣ family of receptors (1, 4, 8). p75 NTR binds all neurotrophins, including brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and NT-4/5. NGF-TrkA signaling is involved in some inflammatory effects of NGF (50), including sensitization of nociceptive afferents and the release of neuropeptides. TrkA expression is increased in bladder afferent cells in lumbosacral dorsal root ganglia (DRG) with acute and chronic cyclophosphamide (CYP)-induced bladder inflammation (51). In addition, p75 NTR expression is also significantly upregulated in bladder afferent cells (2.4-to 2.8-fold) in lumbosacral DRG after CYP-induced cystitis (39).The pan-neurotrophin receptor p75 NTR exhibits a ubiquitous distribution and has many functions and multiple binding partners and ligands (4,8). In the absence of Trk expression, p75NTR is suggested to be involved in apoptosis and regulation of neuronal growth (4, 27); however, in the presence of TrkA, p75 NTR is suggested to function by enhancing Trk binding to neurotrophins (3,4,70). p75 NTR expression has previously been identified in the urinary bladder (61,66,67) but few studies have examined the role of p75 NTR in bladder function or in the context of urinary bladder inflammation (66). Although we do know that p75NTR expression is present in micturition reflex pathways in control rats and is regulated with CYP-induced cystitis (39), the potential role(s) of p75 NTR in urinary bladder reflexes have not been explored. In this study, we determined 1) expression of p75 NTR in the urinary bladder with immunohistochemistry and Western blot and regulation of p75 NTR expression after CYP-induced cystitis, 2) the effect of immunoneutralization with an anti-p75 NTR monoc...

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Section: Discussionmentioning

confidence: 99%

“…It consists of reduced muscle contraction, strength, or velocity and often results in incomplete voiding, postvoid residual, prolonged emptying, and reduced free uroflow (16,17). Detrusor underactivity can be neurogenic, idiopathic, or a result of bladder outflow obstruction (16,17 …”

Section: Discussionmentioning

confidence: 99%

Role of p75^NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

Klinger

Vizzard²

2008

American Journal of Physiology-Renal Physiology

106

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“…Central and post-pontine causes of voiding dysfunctions in the elderly have been previously, if incompletely, characterized. 4,6,[27][28][29][30] The efferent/motor limb of the micturition response operates within the context of a sensory overlay. Normal bladder sensory function is assumed as a requisite for normal storage and micturition.…”

Section: Activation: Alternative Contributors To Detrusor Underactivitymentioning

confidence: 99%

“…5 Human urodynamic data suggest a loss of bladder performance and voiding efficiency with aging. 6,7 Underdiagnosis of DU is not clinically trivial. DU, rather than obstruction, has been found to be etiologic in a significant proportion (23-73%) of symptomatic elderly men, 8,9 an important observation since prostatic procedures intended to relieve obstruction in the presence of DU may be associated with poorer rates of improvement of LUTS and voiding function.…”

Section: Introductionmentioning

confidence: 99%

Aging and the underactive detrusor: A failure of activity or activation?

Smith

2009

Neurourology and Urodynamics

125

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“…Cucchi et al suggested that idiopathic DUA implies two-stage development (i.e. would be preceded by a phase of low detrusor contraction velocity occurring even several months before a decrease in detrusor contraction strength) in adult men [33], an isolated decrease in detrusor contraction velocity observed as the early phase of the process leading to obvious DUA in female patients [34], and that the intrinsic speed of the detrusor may be more sensitive than the intrinsic strength to the factor(s) responsible for DUA [35]. Therefore, it is possible that evaluation of Vdet max would be useful for early diagnosis of DUA and as a good component of examination along with the maximum IVP.…”

Section: Discussionmentioning

confidence: 99%

Effects of Silodosin, an α<sub>1A</sub>-Adrenoceptor Antagonist, and Distigmine, an Acetylcholinesterase Inhibitor, and Their Combined Effects on Impaired Voiding Function in Zucker Diabetic Fatty Rats

et al. 2015

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Background/Aims: To evaluate the effects of silodosin (α_1A-adrenoceptor antagonist) and distigmine (acetylcholinesterase inhibitor), alone or in combination, on voiding dysfunction in Zucker diabetic fatty (ZDF) rats, a type 2 diabetes model, by pressure flow study. Methods: Male ZDF rats were anesthetized with urethane and a catheter was implanted into the bladder through the dome. Saline was continuously infused into the bladder at 6 ml/h to induce the micturition reflex. Intravesical pressure and micturition volume were recorded continuously and various urodynamic parameters were calculated using a waveform analysis system. Results: Increased bladder capacity, residual volume, and urethral resistance and decreased maximum detrusor contraction velocity and urine flow rate, considered to be detrusor underactivity-like symptoms, were observed in ZDF rats. Although both silodosin and distigmine improved impaired voiding function, administration of both drugs in combination was more effective than either drug alone. Conclusions: ZDF rats showed symptoms suggestive of detrusor underactivity, and silodosin tended to ameliorate these symptoms in ZDF rats. These results suggested that an α_1A-adrenoceptor antagonists may be effective against the voiding disorder accompanying not only bladder outlet obstruction but also deficiency of bladder function. Moreover, combined administration of an α_1A-adrenoceptor antagonist with an acetylcholinesterase inhibitor may have additive efficacy in clinical use.

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Development of Idiopathic Detrusor Underactivity in Women: From Isolated Decrease in Contraction Velocity to Obvious Impairment of Voiding Function

Cited by 37 publications

References 12 publications

Role of p75^NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

Role of p75^NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

Aging and the underactive detrusor: A failure of activity or activation?

Effects of Silodosin, an α<sub>1A</sub>-Adrenoceptor Antagonist, and Distigmine, an Acetylcholinesterase Inhibitor, and Their Combined Effects on Impaired Voiding Function in Zucker Diabetic Fatty Rats

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Development of Idiopathic Detrusor Underactivity in Women: From Isolated Decrease in Contraction Velocity to Obvious Impairment of Voiding Function

Cited by 37 publications

References 12 publications

Role of p75NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

Role of p75NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

Aging and the underactive detrusor: A failure of activity or activation?

Effects of Silodosin, an α<sub>1A</sub>-Adrenoceptor Antagonist, and Distigmine, an Acetylcholinesterase Inhibitor, and Their Combined Effects on Impaired Voiding Function in Zucker Diabetic Fatty Rats

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Product

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Role of p75^NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

Role of p75^NTR in female rat urinary bladder with cyclophosphamide-induced cystitis