title: Changes in cholinergic and purinergic neurotransmission in pathologic bladder of chronic spinal rabbit.
abstract: OBJECTIVE
  We evaluated the changes in cholinergic and purinergic neurotransmission in pathologic bladder of chronic spinal rabbits.
  
  
  METHODS
  Detrusor muscle strips were obtained from normal rabbits and chronic spinal rabbits with detrusor hyperreflexia and detrusor sphincter dyssynergia (DSD). Muscle strips were mounted in an organ bath, and transmural nerve electrical field stimulation (EFS: supamaximal voltage, 0.5 msec. duration, 10 second trains) was performed. The responses to EFS and agonists were determined by recording the isometric tension of muscle strips.
  
  
  RESULTS
  Both normal and pathologic detrusor strips contracted in a frequency dependent fashion in response to transmural electrical nerve stimulation. At each frequency, atropine reduced the nerve-mediated contraction in a dose-dependent fashion and left an atropine-resistant response at a concentration of 1 microM. The atropine-resistant contraction was abolished by desensitization of P2X-purinoceptors with repeated exposure to alpha, beta-methylene ATP (10 microM). The atropine sensitive (cholinergic) and resistant (purinergic) contractions increased with an increase in frequency and reached maximum at 20 Hz. The relative contribution of cholinergic and purinergic transmission to the nerve-mediated contraction was determined at this frequency. In normal detrusor, the cholinergic and purinergic components were approximately 40% and 60%. In pathologic detrusor, the cholinergic component increased to 75% whereas the purinergic component decreased to 25%. Exogenously administered acetylcholine and ATP produced dose-dependent contractions of detrusor strips. The concentration-response curves for each agonist did not show significant differences between normal and pathologic detrusor.
  
  
  CONCLUSIONS
  These results suggest that neurotransmission is shifted to a cholinergic dominance in pathologic rabbit bladder affected by detrusor hyperreflexia and DSD.
authors.affiliation: Department of Urology, Fukushima Medical College, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yokota
authors.forename: O
authors.initials: O
authors.lastname: Yamaguchi
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002908:Chronic Disease; D004305:Dose-Response Relationship, Drug; D066298:In Vitro Techniques; D007796:Laminectomy; D008297:Male; D018727:Muscarinic Antagonists; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000294:innervation / Q000503:physiopathology; D011817:Rabbits; D011941:Receptors, Adrenergic / Q000187:drug effects* / Q000502:physiology; D011983:Receptors, Purinergic / Q000187:drug effects* / Q000502:physiology; D012021:Reflex, Abnormal; D001743:Urinary Bladder / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D001745:Urinary Bladder Diseases / Q000209:etiology / Q000503:physiopathology*
chemical_list: D018727:Muscarinic Antagonists; D011941:Receptors, Adrenergic; D011983:Receptors, Purinergic; D001285:Atropine; D000255:Adenosine Triphosphate; D000109:Acetylcholine