MP4-04 URINE STORAGE DYSFUNCTION IN RATS WITH SALT-LOADING HYPERTENSION DEPENDS ON INCREASE IN ATP AND PGE2 RELEASE FROM THE UROTHELIUM

Abstract

You have accessJournal of UrologyUrodynamics/Incontinence/Female Urology: Basic Research II1 Apr 2014MP4-04 URINE STORAGE DYSFUNCTION IN RATS WITH SALT-LOADING HYPERTENSION DEPENDS ON INCREASE IN ATP AND PGE2 RELEASE FROM THE UROTHELIUM Tetsuyuki Kurokawa, Keiko Nagase, Xinmin Zha, and Osamu Yokoyama Tetsuyuki KurokawaTetsuyuki Kurokawa More articles by this author , Keiko NagaseKeiko Nagase More articles by this author , Xinmin ZhaXinmin Zha More articles by this author , and Osamu YokoyamaOsamu Yokoyama More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2014.02.204AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Lifestyle factors, especially hypertension (HT) can influence lower urinary tract functions. HT is one of the risk factors for worsening lower urinary tract symptoms and decreasing the improvement of storage symptoms by α1-blocker. The spontaneous hypertensive rat is considered as a valuable tool for exploring the pathogenesis of detrusor overactivity, but pathological changes in the bladder are thought to be irreversible. It has not yet been determined whether salt sensitive HT contributes to lower urinary tract dysfunction. We investigated the underlying mechanisms of urine storage dysfunction in rats with HT caused by salt loading. METHODS The sympathetic nerve activity is augmented with salt loading in Dahl salt sensitive rats (DSr), but not in Dahl salt resistant rats (DRr). Six-week-old male DSr and DRr were fed with a normal (0.252%) or high-salt (8%) diet and 35 ml water/day for 12 weeks. Blood pressure was measured through the tail artery in a non-anesthetized state. Urine volume and frequency were recorded all day long in a metabolic cage. We calculated the inactive period (sleeping) urine volume ratio, which was defined as urine volume during inactive period divided by 24 h urine output. Whole bladders were excised from 18 week rats and distended in organ bath with Krebs solution. Adenosine triphosphate (ATP) and prostaglandin E2 (PGE2) release from the distended bladder epithelium were measured. Furthermore, changes in surface bladder blood flow were determined with a laser speckle blood flow imaging system (Omegazone OZ-1; Omegawave, Tokyo) . RESULTS In the inactive period, the mean voided volume gradually increased in DRr fed with a normal or high salt diet, while it did not change in DSr fed with a high-salt diet. There were significant differences in mean voided volume after 10 week salt loading between DRr and DSr fed with a high-salt diet. Bladder distension significantly increased ATP and PGE2 release from the urothelium in DSr rats fed a high-salt diet when compared to other 3 group. Bladder blood flow in DSr fed with a high-salt diet was found to decrease, when compared to DSr fed with a normal diet. CONCLUSIONS These results indicate that salt loading induces HT and decreases the voided volume possibly via excitatory effects of ATP and PGE2 from the epithelium on bladder afferent nerves. Increases in mediator release from the epithelial are believed to depend on the bladder ischemia caused by HT. This model is useful in defining the mechanisms governing the induction of storage dysfunction in patients with HT. © 2014FiguresReferencesRelatedDetails Volume 191Issue 4SApril 2014Page: e43 Advertisement Copyright & Permissions© 2014MetricsAuthor Information Tetsuyuki Kurokawa More articles by this author Keiko Nagase More articles by this author Xinmin Zha More articles by this author Osamu Yokoyama More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...