title: Diphosphate regulation of adenosine triphosphate sensitive potassium channel in human bladder smooth muscle cells.
abstract: OBJECTIVE
  To clarify the properties of adenosine triphosphate sensitive K+ channel in human detrusor smooth muscle we examined the effect of the representative nicotinic acid derivatives β-nicotinamide adenine dinucleotide, cyclic adenosine diphosphate ribose and nicotinic acid adenine dinucleotide phosphate (Sigma-Aldrich®) on human detrusor adenosine triphosphate sensitive K+ channels.
  
  
  METHODS
  Patch clamp procedures were done in human detrusor cells. Reverse transcriptase and real-time polymerase chain reaction were performed to clarify the subunit components of adenosine triphosphate sensitive K+ channels.
  
  
  RESULTS
  The K+ channel opener levcromakalim induced a long lasting outward current that was inhibited by glibenclamide (Sigma-Aldrich) under the whole cell configuration. The single channel study revealed that the unitary conductance of the adenosine triphosphate sensitive K+ channel in the human detrusor was 11 pS and nucleotide diphosphates increased its open probability. Applying β-nicotinamide adenine dinucleotide also activated the adenosine triphosphate sensitive K+ channel but applying cyclic adenosine diphosphate ribose or nicotinic acid adenine dinucleotide phosphate had little effect on channel activation. Molecular studies indicated that Kir6.1 and SUR2B were the predominant components of the adenosine triphosphate sensitive K+ channel in the human detrusor.
  
  
  CONCLUSIONS
  To our knowledge we report the first single channel study of the adenosine triphosphate sensitive K+ channel in the human detrusor. The properties of this channel, ie unitary conductance, adenosine triphosphate sensitivity and diphosphate activation, were consistent with those of other smooth muscle organs. β-Nicotinamide adenine dinucleotide has the potency to activate adenosine triphosphate sensitive K+ channels in the human detrusor. This channel likely has some role during ischemic conditions as well as physiological muscle motion leading to the activation of cell metabolism.
authors.affiliation: Department of Urology, Graduate School of Medical Sciences, Kyushu University, and Special Patient Oral Care Unit, Kyushu University Hospital, Fukuoka, Japan.
authors.forename: Shunichi
authors.initials: S
authors.lastname: Kajioka
authors.forename: Nouval
authors.initials: N
authors.lastname: Shahab
authors.forename: Haruhiko
authors.initials: H
authors.lastname: Asano
authors.forename: Hiromitsu
authors.initials: H
authors.lastname: Morita
authors.forename: Megumi
authors.initials: M
authors.lastname: Sugihara
authors.forename: Fumi
authors.initials: F
authors.lastname: Takahashi-Yanaga
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Yoshihara
authors.forename: Shinsuke
authors.initials: S
authors.lastname: Nakayama
authors.forename: Narihito
authors.initials: N
authors.lastname: Seki
authors.forename: Seiji
authors.initials: S
authors.lastname: Naito
mesh_terms: D000368:Aged; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D054086:KATP Channels / Q000502:physiology*; D008297:Male; D009130:Muscle, Smooth / Q000166:cytology* / Q000502:physiology*; D001743:Urinary Bladder / Q000502:physiology*
chemical_list: D054086:KATP Channels