title: Effects of prostaglandin E1 on vascular ATP-sensitive potassium channels.
abstract: BACKGROUND
  Prostaglandin E1 (PGE1) has been reported to activate ATP-sensitive potassium (KATP) channels, which induces vasorelaxation. However, direct evidence of PGE1 interactions with vascular KATP channels is limited.
  
  
  METHODS
  The present study investigated the effects and mechanisms of PGE1 on vascular KATP channels in both isometric tension and patch clamp experiments. Isometric tension experiments were performed in rat thoracic aortic rings without an endothelium. Electrophysiologic experiments were performed using patch-clamp techniques to monitor KATP channels in rat vascular smooth muscle cells.
  
  
  RESULTS
  PGE1 significantly decreased the isometric tension in a concentration-dependent manner, which was partially inhibited by pretreating with a KATP channel inhibitor, glibenclamide (1 microM), or an inhibitor of protein kinase A (PKA), Rp-cAMPS (100 microM). Application of PGE1 to the bath solution during cell-attached recordings induced a significant increase in KATP channel activity, whereas PGE1 failed to activate KATP channels in the inside-out patches. The PGE1-induced KATP channel currents in cell-attached patches were abolished by pretreating with Rp-cAMPS (100 microM).
  
  
  CONCLUSIONS
  The results indicate that the activation of vascular KATP channels played an important role in the PKA-dependent PGE1-induced vasorelaxation. Furthermore, an electrophysiological experiment demonstrated that PGE1 activated vascular KATP channels via PKA activation.
authors: Department of Dental Anesthesiology, Tokushima University School of Dentistry, Tokushima, Japan.
authors: Satoru
authors: S
authors: Eguchi
authors: Takashi
authors: T
authors: Kawano
authors: Yinhua
authors: Katsuya
authors: K
authors: Tanaka
authors: Sonoko
authors: S
authors: Yasui
authors: Kazuaki
authors: K
authors: Mawatari
authors: Akira
authors: A
authors: Takahashi
authors: Yutaka
authors: Y
authors: Nakaya
authors: Shuzo
authors: S
authors: Oshita
authors: Nobuyoshi
authors: N
authors: Nakajo
mesh_terms: D000465:Algorithms; D000527:Alprostadil / Q000494:pharmacology*; D000704:Analysis of Variance; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000031:analogs & derivatives / Q000494:pharmacology; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors; D004305:Dose-Response Relationship, Drug; D005905:Glyburide / Q000494:pharmacology; D066298:In Vitro Techniques; D054086:KATP Channels / Q000502:physiology*; D008297:Male; D018408:Patch-Clamp Techniques; D010656:Phenylephrine / Q000494:pharmacology; D020110:Pinacidil / Q000494:pharmacology; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013873:Thionucleotides / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D054086:KATP Channels; D047428:Protein Kinase Inhibitors; D013873:Thionucleotides; D014665:Vasodilator Agents; D005576:Colforsin; D010656:Phenylephrine; C016957:adenosine-3',5'-cyclic phosphorothioate; D020110:Pinacidil; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D000527:Alprostadil; D005905:Glyburide