title: Altered function of inward rectifier potassium channels in cerebrovascular smooth muscle after ischemia/reperfusion.
abstract: OBJECTIVE
  Several recent studies have demonstrated that inward rectifier potassium channels (K(ir)s) are located on vascular smooth muscle of cerebral arteries in the rat. Activation of the K(ir)s dilates the arteries by relaxing the vascular smooth muscle. We tested the following hypothesis in the present study: function of inward rectifier potassium channels is altered after ischemia/reperfusion (I/R).
  
  
  METHODS
  Temporary (2-hour) focal ischemia was induced in male Long-Evans rats (3% isoflurane anesthesia) by the intraluminal filament model. After 24 hours of reperfusion, ipsilateral and contralateral middle cerebral arteries (MCAs) were harvested and mounted on micropipettes, pressurized to 85 mm Hg, and luminally perfused.
  
  
  RESULTS
  Resting diameters for contralateral (control) and ipsilateral (I/R) MCAs were not significantly different (215+/-4 microm and 211+/-5 microm [n = 6 and n = 7], respectively). Activation of the K(ir)s by abluminal administration of 15 mmol/L KCl to the control MCAs dilated the MCA by 34+/-4% (n = 8). Activation of the K(ir)s in I/R MCAs produced a dilation of only 11+/-3% (n = 8; P<0.001 compared with control). BaCl2 (75 micromol/L), a concentration-selective inhibitor of the K(ir)s, significantly attenuated the dilation produced by 15 mmol/L KCl in control MCAs but not in the I/R MCAs. Endothelial-mediated dilations elicited by the luminal administration of uridine triphosphate (10 micromol/L) produced similar dilations in both groups (32+/-5% for sham [n = 4] and 33+/-2% for I/R [n = 4]), indicating that dilator function in general was not altered in I/R vessels.
  
  
  CONCLUSIONS
  We conclude that Kir function is altered after I/R. The Kir altered function is likely to exacerbate the brain injury occurring after I/R.
authors.affiliation: Department of Anesthesiology, Baylor College of Medicine, Houston, Tex 77030, USA.
authors.forename: S P
authors.initials: SP
authors.lastname: Marrelli
authors.forename: T D
authors.initials: TD
authors.lastname: Johnson
authors.forename: A
authors.initials: A
authors.lastname: Khorovets
authors.forename: W F
authors.initials: WF
authors.lastname: Childres
authors.forename: R M
authors.initials: RM
authors.lastname: Bryan
mesh_terms: D000818:Animals; D017609:Barium Compounds / Q000494:pharmacology; D002545:Brain Ischemia / Q000378:metabolism*; D002536:Cerebral Arteries / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D002712:Chlorides / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000502:physiology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000378:metabolism*; D024661:Potassium Channels, Inwardly Rectifying; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D015424:Reperfusion; D014544:Uridine Triphosphate / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D017609:Barium Compounds; D002712:Chlorides; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; C024986:barium chloride; D011189:Potassium Chloride; D014544:Uridine Triphosphate