title: Role of K+ channels in regulating spontaneous activity in detrusor smooth muscle in situ in the mouse bladder.
abstract: OBJECTIVE
  We investigated the functional role of K(+) channels for regulating spontaneous activity in mouse bladder detrusor smooth muscle.
  
  
  METHODS
  The effects of different K(+) channels blockers on spontaneous changes in membrane potential and intracellular Ca(2+) dynamics were examined using intracellular recording techniques and Ca(2+) imaging with fluo-4 fluorescence, respectively.
  
  
  RESULTS
  Detrusor smooth muscle generated spontaneous action potentials and Ca(2+) transients. Iberiotoxin (0.1 microM), charybdotoxin (0.1 microM) or tetraethylammonium (1 mM) increased the amplitude of action potentials and prolonged their repolarizing phase without inhibiting their after-hyperpolarization. Tetraethylammonium (10 mM) but not stromatoxin (0.1 microM) suppressed after-hyperpolarization and further increased the amplitude and half duration of action potentials. Apamin (0.1 microM) increased the frequency of action potentials but had no effect on their configuration. Spontaneous Ca(2+) transients were generated in individual detrusor smooth muscle cells and occasionally propagated to neighboring cells to form intercellular Ca(2+) waves. Transmural nerve stimulations invariably initiated synchronous Ca(2+) transients within and across muscle bundles. Charybdotoxin (0.1 microM) increased the amplitude of spontaneous Ca(2+) transients, while the subsequent application of tetraethylammonium (10 mM) increased their half duration. In addition, tetraethylammonium increased the synchronicity of Ca(2+) transients in muscle bundles.
  
  
  CONCLUSIONS
  These results suggest that large and intermediate conductance Ca(2+) activated K(+) channels contribute to action potential repolarization and restrict the excitability of detrusor smooth muscle in the mouse bladder. In addition, the activation of voltage dependent K(+) channels is involved in repolarization and after-hyperpolarization, and it has a fundamental role in stabilizing detrusor smooth muscle excitability.
authors.affiliation: Department of Nephro-Urology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
authors.forename: Masa
authors.initials: M
authors.lastname: Hayase
authors.forename: Hikaru
authors.initials: H
authors.lastname: Hashitani
authors.forename: Kenjiro
authors.initials: K
authors.lastname: Kohri
authors.forename: Hikaru
authors.initials: H
authors.lastname: Suzuki
mesh_terms: D000200:Action Potentials; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D004594:Electrophysiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D023421:Models, Animal; D009119:Muscle Contraction / Q000502:physiology; D009130:Muscle, Smooth / Q000502:physiology*; D026902:Potassium Channel Blockers / Q000494:pharmacology*; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D012680:Sensitivity and Specificity; D001743:Urinary Bladder / Q000502:physiology*
chemical_list: D015220:Calcium Channels; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D001030:Apamin