You have accessJournal of UrologyUrodynamics/Incontinence/Female Urology: Basic Research (1)1 Apr 201321 RECEPTORS INVOLVED IN PUDENDAL INHIBITION OF THE MICTURITION REFLEX Abhijith Mally, Yosuke Matsuta, Fan Zhang, Bing Shen, Jicheng Wang, James Roppolo, William de Groat, and Changfeng Tai Abhijith MallyAbhijith Mally Pittsburgh, PA More articles by this author , Yosuke MatsutaYosuke Matsuta Pittsburgh, PA More articles by this author , Fan ZhangFan Zhang Pittsburgh, PA More articles by this author , Bing ShenBing Shen Pittsburgh, PA More articles by this author , Jicheng WangJicheng Wang Pittsburgh, PA More articles by this author , James RoppoloJames Roppolo Pittsburgh, PA More articles by this author , William de GroatWilliam de Groat Pittsburgh, PA More articles by this author , and Changfeng TaiChangfeng Tai Pittsburgh, PA More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2013.02.1396AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES To determine the role of opioid and metabotropic glutamate 5 receptors (mGluR5) in pudendal inhibition of bladder overactivity. METHODS Cystometrograms (CMGs) were performed in 11 cats under alpha-chloralose anesthesia by slowly infusing the bladder with saline or 0.25% acetic acid (AA). Pudendal nerve stimulation at intensities of multiple times the threshold (T) to induce observable anal twitching was applied during CMGs to inhibit the bladder overactivity induced by AA irritation. Naloxone (0.1, 0.3, and 1 mg/kg, i.v.) was administered to block opioid receptors followed by MTEP (3 and 10 mg/kg, i.v.) administration to block mGluR5 receptors. After each dose of drug, pudendal inhibition of bladder overactivity was examined during CMGs. RESULTS AA irritated the bladder, induced bladder overactivity, and significantly (P<0.0001) reduced bladder capacity to 23.6±2.7%% of saline control capacity. Pudendal nerve stimulation at 1-1.5T and 4T suppressed bladder overactivity and significantly increased the capacity to 57.5±8.1% (P=0.0005) and 106±15% (P=0.0002), respectively, of the saline control capacity. Naloxone had no effect on pudendal inhibition, but MTEP eliminated the inhibition induced by low intensity stimulation and significantly (P<0.05) reduced the inhibition induced by high intensity stimulation. Neither naloxone or MTEP altered baseline bladder overactivity. CONCLUSIONS Opioid receptors are not involved in pudendal inhibition of bladder overactivity, but mGluR5 receptors are partially involved. Understanding neurotransmitter mechanisms could improve the efficacy of neuromodulation therapy for overactive bladder (OAB) treatment, and identify molecular targets for development of new drugs for treating OAB. © 2013 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 189Issue 4SApril 2013Page: e8 Advertisement Copyright & Permissions© 2013 by American Urological Association Education and Research, Inc.MetricsAuthor Information Abhijith Mally Pittsburgh, PA More articles by this author Yosuke Matsuta Pittsburgh, PA More articles by this author Fan Zhang Pittsburgh, PA More articles by this author Bing Shen Pittsburgh, PA More articles by this author Jicheng Wang Pittsburgh, PA More articles by this author James Roppolo Pittsburgh, PA More articles by this author William de Groat Pittsburgh, PA More articles by this author Changfeng Tai Pittsburgh, PA More articles by this author Expand All Advertisement Advertisement PDF DownloadLoading ...