MP08-03 BRAIN HYDROGEN SULFIDE SUPPRESSES THE RAT MICTURITION REFLEX VIA BRAIN GABA RECEPTORS

Abstract

You have accessJournal of UrologyBladder & Urethra: Anatomy, Physiology & Pharmacology (MP08)1 Sep 2021MP08-03 BRAIN HYDROGEN SULFIDE SUPPRESSES THE RAT MICTURITION REFLEX VIA BRAIN GABA RECEPTORS Masaki Yamamoto, Takahiro Shimizu, Suo Zou, Shogo Shimizu, Youichirou Higashi, Mikiya Fujieda, and Motoaki Saito Masaki YamamotoMasaki Yamamoto More articles by this author , Takahiro ShimizuTakahiro Shimizu More articles by this author , Suo ZouSuo Zou More articles by this author , Shogo ShimizuShogo Shimizu More articles by this author , Youichirou HigashiYouichirou Higashi More articles by this author , Mikiya FujiedaMikiya Fujieda More articles by this author , and Motoaki SaitoMotoaki Saito More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000001981.03AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: We previously reported that hydrogen sulfide (H2S), an endogenous gasotransmitter, is a possible relaxation factor in the rat bladder. However, roles of central H2S in regulation of the micturition reflex are unknown. In this study, we examined effects of centrally administered GYY4137 (GYY, H2S donor) and AOAA (H2S synthesis inhibitor) on the rat micturition reflex. METHODS: Urethane anesthetized (0.8 g/kg, ip) male Wistar rats (350-400 g) were used. A catheter was inserted into the bladder to perform continuous cystometry (12 ml/h saline infusion). Three hours after the surgery, GYY (3 or 10 nmol/rat), AOAA (30 or 100 μg/rat) or vehicle was intracerebroventricularly (ICV) administered. In some rats, effects of ICV pretreated SR95531 (SR, GABAA antagonist, 0.1 nmol/rat) or SCH50911 (SCH, GABAB antagonist, 0.1 nmol/rat) on the GYY (10 nmol/rat, ICV)-induced responses were investigated. Continuous cystometry and evaluation of intercontraction intervals (ICI) and maximal voiding pressure (MVP) were started 60 min before the first ICV administration. In some rats, before and after AOAA administration (30 μg/rat, ICV), single cystometry (12 ml/h saline infusion) was performed. RESULTS: GYY dose-dependently prolonged ICI without changing MVP (fig. 1A-B). On the other hand, AOAA significantly shortened ICI without changing MVP (fig. 1C-D). In single cystometry, AOAA significantly reduced single-voided volume and bladder capacity without increasing post-voiding residual volume or voiding efficiency (table 1). The AOAA (30 μg/rat, ICV)-induced ICI shortening was reversed in the central presence of GYY (10 nmol/rat, ICV) (data not shown). The GYY-induced ICI prolongation was suppressed by SR and SCH (fig. 2A-B). CONCLUSIONS: Brain H2S endogenously suppresses the rat micturition reflex via brain GABAA and GABAB receptors in rats. Thus, the brain H2S might be new therapeutic targets for neurogenic bladder overactivity. Source of Funding: JSPS KAKENHI (#17K09303, #20K07827), Takeda Science Foundation © 2021 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 206Issue Supplement 3September 2021Page: e150-e150 Advertisement Copyright & Permissions© 2021 by American Urological Association Education and Research, Inc.MetricsAuthor Information Masaki Yamamoto More articles by this author Takahiro Shimizu More articles by this author Suo Zou More articles by this author Shogo Shimizu More articles by this author Youichirou Higashi More articles by this author Mikiya Fujieda More articles by this author Motoaki Saito More articles by this author Expand All Advertisement Loading ...