MP77-09 CHRONIC PSYCHOLOGICAL STRESS LEADS TO BLADDER HYRALGESIA VIA STRESS INDUCED SENSITIZATION OF C FIBERS AND MECHANORECPTORS

Abstract

You have accessJournal of UrologyUrodynamics/Lower Urinary Tract Dysfunction/Female Pelvic Medicine: Non-neurogenic Voiding Dysfunction II1 Apr 2016MP77-09 CHRONIC PSYCHOLOGICAL STRESS LEADS TO BLADDER HYRALGESIA VIA STRESS INDUCED SENSITIZATION OF C FIBERS AND MECHANORECPTORS Yunliang Gao, Rong Zhang, Huiyi Chang, and Larissa Rodriguez Yunliang GaoYunliang Gao More articles by this author , Rong ZhangRong Zhang More articles by this author , Huiyi ChangHuiyi Chang More articles by this author , and Larissa RodriguezLarissa Rodriguez More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2016.02.1923AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Patients affected by overactive bladder and painful bladder syndrome/interstitial cystitis report symptoms exacerbation when stressed. We have shown that anxiety prone animals exposed to chronic psychological water avoidance stress (WAS) develop sustained bladder hyperalgesia. The bladder cooling reflex (BCR) is a segmental reflex believed to be triggered by cold receptors in bladder wall with C fibers signaling. We aimed to evaluate the chronic stress induces changes in BCR and if C fiber sensitization contributes to stress-induced bladder hypersensitivity. METHODS 22 adult female Wistar-Kyoto rats equally divided to 10-day WAS or handled controls. On day 11, animals were evaluated by cystometrogram (CMG) as well as visceromotor reflex (VMR) for bladder sensitivity and pain to saline infusion. CMG and VMR were obtained during bladder infusion at room temperature (RT) and cold (4 degree C) with an open urethral outlet thus allowing the animal to void. CMG and VMR were also obtained during RT isotonic bladder distention (RT-IBD, 10-40 cmH2O) with urethral occlusion. RESULTS During RT infusion, WAS rats had a significant decreases in pressure threshold (PT) and the ratio of VMR threshold/maximum intravesical pressure (IVPmax). VMR duration significantly increased in WAS. BCR induced a more dramatic significant decline in PT and the ratio of VMR threshold/IVPmax in WAS (Fig.1A). No significant differences were found in contraction duration, inter-contraction interval or the VMR area under the curve (AUC) and duration. At RT-IBD (Fig.1B-C), VMR latency in WAS significantly decreased compared to controls. At 20 cmH2O, VMR AUC in WAS significantly increased compared to controls. CONCLUSIONS Chronic psychological stress induces bladder hypersensitivity, which manifests as earlier voiding and VMR. Prolonged VMR duration in WAS correlates with increased bladder sensitivity during voiding. BCR evokes C fibers activation and suggests that stress induced bladder hypersensitivity in functional voiding disorders mediated in part by afferent sensitization. Earlier VMR appearance at RT-IBD suggests a role for mechanoreceptor sensitivity in stress-induced bladder hypersensitivity. © 2016FiguresReferencesRelatedDetails Volume 195Issue 4SApril 2016Page: e1018-e1019 Advertisement Copyright & Permissions© 2016MetricsAuthor Information Yunliang Gao More articles by this author Rong Zhang More articles by this author Huiyi Chang More articles by this author Larissa Rodriguez More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...