title: Purinergic activation of a leak potassium current in freshly dissociated myocytes from mouse thoracic aorta.
abstract: OBJECTIVE
  Exogenous ATP elicits a delayed calcium-independent K(+) current on freshly isolated mouse thoracic aorta myocytes. We investigated the receptor, the intracellular pathway and the nature of this current.
  
  
  METHODS
  The patch-clamp technique was used to record ATP-elicited delayed K(+) current in freshly dissociated myocytes.
  
  
  RESULTS
  ATP-elicited delayed K(+) current was not inhibited by a 'cocktail' of K(+) channel blockers (4-AP, TEA, apamin, charybdotoxin, glibenclamide). The amplitude of the delayed K(+) current decreased after the reduction of extracellular pH from 7.4 to 6.5. These two characteristics suggest that this current could be carried by the TASK subfamily of 'twin-pore potassium channels' (K2P). Purinergic agonists including dATP, but not ADP, activated the delayed K(+) current, indicating that P2Y(11) is the likely receptor involved in its activation. The PKC activator phorbol ester 12,13-didecanoate stimulated this current. In addition, the PKC inhibitor Gö 6850 partially inhibited it. Real-time quantitative PCR showed that the genes encoding TASK-1 and TASK-2 are expressed.
  
  
  CONCLUSIONS
  Our results indicate that blocker cocktail-insensitive delayed K(+) current in freshly dissociated aortic myocytes is probably carried by the TASK subfamily of twin-pore channels.
authors.affiliation: Department of Zoology and Animal Biology, University of Geneva, Sciences III, Geneva, Switzerland.
authors.forename: S
authors.initials: S
authors.lastname: Hayoz
authors.forename: R
authors.initials: R
authors.lastname: Bychkov
authors.forename: K
authors.initials: K
authors.lastname: Serir
authors.forename: M
authors.initials: M
authors.lastname: Docquier
authors.forename: J-L
authors.initials: JL
authors.lastname: Bény
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001013:Aorta, Thoracic; D001030:Apamin / Q000494:pharmacology; D018999:Charybdotoxin / Q000494:pharmacology; D015870:Gene Expression; D005905:Glyburide / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D007211:Indoles / Q000494:pharmacology; D008297:Male; D008301:Maleimides / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D032342:Muscle Cells / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024683:Potassium Channels, Tandem Pore Domain / Q000235:genetics / Q000378:metabolism*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods
chemical_list: D007211:Indoles; C498739:Kcnk5 protein, mouse; D008301:Maleimides; D009419:Nerve Tissue Proteins; D026902:Potassium Channel Blockers; D024683:Potassium Channels, Tandem Pore Domain; D018999:Charybdotoxin; C420132:potassium channel subfamily K member 3; D001030:Apamin; D000255:Adenosine Triphosphate; D011493:Protein Kinase C; C070515:bisindolylmaleimide I; D005905:Glyburide