Abstract

ATP is an important mediator of urgency in women with detrusor overactivity (DO). In order to understand how different degrees of bladder stretch elicited ATP release in DO patients compared with controls, sequential aliquots were collected during cystometry and ATP release was measured at each degree of bladder filling, in female patients with DO and controls. In both DO and control groups, ATP release was induced during bladder filling, suggesting that stretch stimulated further ATP release. However, the luminal ATP concentrations were already high at early filling stage (200 mL), which was even greater than those at the later filling stages (400 mL and maximum cystometric capacity, MCC), indicating that a substantial ATP release has been induced during early filling (200 mL) in both DO and controls. In DO, ATP release at 200 mL was significantly higher in those with low first desire to void (FDV) (≤200 mL) than in those with higher FDV (>200 mL); this may suggest that ATP release at early stretch may play an important role in urgency (early sensation) in DO. ATP concentrations remained unchanged after voiding, suggesting that voiding did not further induce ATP release into intraluminal fluid.

Highlights

  • The urothelium, which was once regarded as an inert, protective barrier, plays a key role in bladder sensory and motor functions [1]

  • Adenosine triphosphate CSU (ATP) release is induced by urothelial stretch during bladder filling, it is unclear whether stretch-induced ATP is involved in triggering bladder contraction, either at physiological maturation or during pathological conditions such as detrusor overactivity (DO), and the pattern of ATP release in human bladder and its association with bladder sensation have not been clearly understood

  • For the first time ATP release during bladder filling has been investigated in sequential intraluminal fluid samples in female patients with or without DO

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Summary

Introduction

The urothelium, which was once regarded as an inert, protective barrier, plays a key role in bladder sensory and motor functions [1]. The hypothesis that the purine nucleotide ATP is a neurotransmitter responsible for nonadrenergic, noncholinergic neurotransmission was proposed in 1972 and termed purinergic signalling [2]. Both animal and human studies show that nonneuronal ATP is released from the bladder urothelium in response to stretch [3,4,5,6]. Intravesical application of ATP has been shown to induce detrusor overactivity [7] Urothelial derived mediators, such as acetylcholine and ATP, signal the sensation of bladder fullness to the central nervous system, triggering the micturition reflex [8]. OAB was shown to be associated with increased ATP release [11, 12]

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