title: Changed responsiveness of the detrusor in rabbits with alloxan induced hyperglycemia: possible role of 5-hydroxytryptamine for diabetic bladder dysfunction.
abstract: OBJECTIVE
  We assessed whether the responsiveness of the detrusor is changed in rabbits with alloxan induced hyperglycemia.
  
  
  METHODS
  Hyperglycemia was induced by a bolus intravenous injection of alloxan (60 mg./kg.) in Japanese White male rabbits. At 16 weeks after alloxan detrusor muscle strips prepared from age matched normoglycemic and hyperglycemic rabbits were mounted in organ chambers. Contractile responses to KCl, carbachol, adenosine triphosphate, 5-hydroxytryptamine and electrical field stimulation were compared in the 2 groups. The effect of sarpogrelate as a selective antagonist of 5-hydroxytryptamine 2A receptor on the contractile response to 5-hydroxytryptamine was also compared.
  
  
  RESULTS
  The current experiments demonstrated that hyperglycemia caused significant decreases in neurogenic and carbachol induced contractions accompanied by unchanged adenosine triphosphate and KCl induced contractions. Neurogenic bladder contraction in the hyperglycemic rabbit was significantly potentiated by exogenously applied 5-hydroxytryptamine. Potentiation was detectable even after the desensitization of purinoceptors but undetectable in the presence of atropine. Hyperglycemia resulted in enhancement of the 5-hydroxytryptamine induced bladder contraction. Sarpogrelate tended to normalize the enhanced contraction.
  
  
  CONCLUSIONS
  The decrease in neurogenic bladder contraction possibly accompanied by the decreased density of muscarinic receptors, the potentiation of neurogenic bladder contraction with 5-hydroxytryptamine probably due to facilitated cholinergic transmission and the enhanced contractility to 5-hydroxytryptamine would be at least in part involved in bladder dysfunction associated with hyperglycemia.
authors.affiliation: Department of Urology, Saitama Medical Center, Saitama Medical School, Kawagoe, Japan.
authors.forename: Nobutaka
authors.initials: N
authors.lastname: Ichiyanagi
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Tsujii
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Masuda
authors.forename: Kazunori
authors.initials: K
authors.lastname: Kihara
authors.forename: Moritaka
authors.initials: M
authors.lastname: Goto
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Azuma
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D003929:Diabetic Neuropathies / Q000503:physiopathology*; D008297:Male; D009122:Muscle Hypertonia / Q000503:physiopathology*; D011817:Rabbits; D011976:Receptors, Muscarinic / Q000502:physiology; D012701:Serotonin / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology; D014521:Urethra / Q000187:drug effects / Q000503:physiopathology*; D001743:Urinary Bladder / Q000187:drug effects / Q000503:physiopathology*; D001750:Urinary Bladder, Neurogenic / Q000503:physiopathology*; D014563:Urodynamics / Q000502:physiology
chemical_list: D011976:Receptors, Muscarinic; D012701:Serotonin