title: Mild hypercapnia induces vasodilation via adenosine triphosphate-sensitive K+ channels in parenchymal microvessels of the rat cerebral cortex.
abstract: BACKGROUND
  Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex.
  
  
  METHODS
  Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 microm) was monitored using computerized videomicroscopy.
  
  
  RESULTS
  During contraction to prostaglandin F2alpha (5 x 10(-7) m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10(-6) m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10(-7) m) as well as the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (10(-4) m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10(-8) to 3 x 10(-7) m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide.
  
  
  CONCLUSIONS
  These results suggest that in parenchymal microvessels of the rat cerebral cortex, decreased pH corresponding with hypercapnia, but not hypercapnia itself, contributes to cerebral vasodilation produced by carbon dioxide and that ATP-sensitive K+ channels play a major role in vasodilator responses produced by mild hypercapnia.
authors.affiliation: Department of Anesthesia, Japanese Red Cross Society, Wakayama Medical Center, Japan.
authors.forename: Katsutoshi
authors.initials: K
authors.lastname: Nakahata
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kinoshita
authors.forename: Yusei
authors.initials: Y
authors.lastname: Hirano
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Kimoto
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Iranami
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Hatano
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001160:Arterioles / Q000502:physiology; D002540:Cerebral Cortex / Q000098:blood supply*; D002560:Cerebrovascular Circulation; D015237:Dinoprost / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000503:physiopathology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D014664:Vasodilation / Q000187:drug effects
chemical_list: D015221:Potassium Channels; D000255:Adenosine Triphosphate; D015237:Dinoprost; D019331:NG-Nitroarginine Methyl Ester