title: Murine in vitro whole bladder model: a method for assessing phenotypic responses to pharmacologic stimuli and hypoxia.
abstract: OBJECTIVE
  Recent advances in genetic manipulation have allowed for over expression or deletion of selective genes in mice. This offers urologic investigators new means of understanding bladder function in the context of normal development or the response to outlet obstruction. It is important to correlate any genetic manipulations in mice with specific phenotypic properties such as voiding patterns, or muscle strip physiology. We describe a simple in vivo whole bladder preparation that may be used to study the phenotypic changes in bladder function.
  
  
  METHODS
  Murine bladders were mounted on a 30 gauge needle and mounted in an organ chamber containing a physiologic buffer solution. Passive bladder properties were assessed with cystometry, and active contractile responses were measured in response to electrical field stimulation and agonists. The effects of hypoxia were also studied.
  
  
  RESULTS
  Compliance in the murine bladder is dependent upon actin myosin interactions, and increased in the presence of calcium free buffer and EGTA. The sarcoplasmic reticulum plays a smaller role in the contraction of murine bladder than in other species. Murine bladder smooth muscle demonstrated a remarkable ability to withstand hypoxia.
  
  
  CONCLUSIONS
  This simple model can be adapted to help study the murine bladder smooth muscle phenotype under highly controlled circumstances.
authors.affiliation: The Children's Hospital of Philadelphia, Division of Urology, Wood Center, Philadelphia, Pennsylvania 19104, USA. Zderic@email.chop.edu
authors.forename: Joel C
authors.initials: JC
authors.lastname: Hutcheson
authors.forename: Raimund
authors.initials: R
authors.lastname: Stein
authors.forename: Samuel
authors.initials: S
authors.lastname: Chacko
authors.forename: Michael
authors.initials: M
authors.lastname: Carr
authors.forename: Douglas A
authors.initials: DA
authors.lastname: Canning
authors.forename: Stephen A
authors.initials: SA
authors.lastname: Zderic
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002021:Buffers; D002614:Chelating Agents / Q000494:pharmacology*; D004533:Egtazic Acid / Q000494:pharmacology*; D004558:Electric Stimulation; D005260:Female; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D007537:Isometric Contraction; D051379:Mice; D008807:Mice, Inbred BALB C; D010641:Phenotype; D011189:Potassium Chloride / Q000494:pharmacology; D011312:Pressure; D001743:Urinary Bladder / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology*; D001748:Urinary Bladder Neck Obstruction / Q000235:genetics / Q000503:physiopathology*; D014563:Urodynamics
chemical_list: D002021:Buffers; D002614:Chelating Agents; D004533:Egtazic Acid; D011189:Potassium Chloride; D001285:Atropine; D000255:Adenosine Triphosphate