Alterations of the myovesical plexus of the human overactive detrusor.

Kamiel A J Kuijpers,John P F A Heesakkers,Jack A Schalken

doi:10.1155/2014/754596

Kamiel A J Kuijpers, John P F A Heesakkers + Show 1 more

Open Access

https://doi.org/10.1155/2014/754596

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Abstract

Objectives. The human bladder shows spontaneous autonomous activity. Detrusor overactivity could be seen as a consequence of exaggerated autonomous activity. Interstitial cells (ICs) play a potential role in coordination of autonomous activity. As it is suggested that changes in ICs coexist with detrusor overactivity (DO), we investigated possible alterations to human bladder ICs. Methods. Biopsies were obtained from 23 patients and were categorized into four groups: genuine stress incontinence (without DO) (n = 5), neurogenic disease with DO (n = 6), bladder outlet obstruction with DO (n = 6), or idiopathic DO (n = 6). Specimens were processed to investigate expression of N-cadherin and PGP9.5. N-cadherin expression was semiquantitatively analyzed and correlated to PG9.5 expression and bladder wall morphology. Results. The population of cells expressing N-cadherin is altered in the overactive detrusor, making no difference between the sources of DO. Punctate distribution of morphological changes was found and downregulation of PGP9.5 expression seemed to coexist with upregulation of N-cadherin expression in the detrusor layer. Conclusions. The population of N-cadherin+ cells of the interstitial compartment of the human bladder has the ability to proliferate. As this proliferation seems to coexist with denervation, it could be possible that a highly developed network of interstitial cells replaces the loss of innervation in overactive detrusor.

Highlights

The overactive bladder (OAB) is a symptomatic diagnosis based on the presence of urgency, with or without incontinence, and is usually accompanied by frequency and nocturia [1]
Relatively little is known about the aetiology of detrusor overactivity (DO), it is clear that the human urinary bladder cannot merely be seen as a passive “black box,” solely controlled by neuronal input
In all patients suffering from OAB, intravesical pressure rises during filling were due to DO, as compliance was normal

Summary

Introduction

The overactive bladder (OAB) is a symptomatic diagnosis based on the presence of urgency, with or without incontinence, and is usually accompanied by frequency and nocturia [1]. Patients with OAB symptoms and detrusor overactivity (DO) can be divided into three groups; those with neuropathic laesions, those with bladder outlet obstruction (BOO), and those with neither (idiopathic DO) [3]. It was found that the isolated bladder shows spontaneous nonneuronal contraction during the filling phase, known as autonomous activity of the bladder [4]. As frequency and urgency occur during this filling phase, DO can be seen as a consequence of exaggerated autonomous activity during the storage of urine [5]

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