title: Vasodilation mediated by inward rectifier K+ channels in cerebral microvessels of hypertensive and normotensive rats.
abstract: Although inward rectifier K+ channels contribute to the regulation of cerebral circulation, dilation of cerebral microvasculature mediated by these channels has not been demonstrated in chronic hypertension. We designed the present study to examine the roles of inward rectifier K+ channels in the vasodilation produced by increased levels of extracellular K+ in cerebral parenchymal arterioles from hypertensive and normotensive rats. During constriction to prostaglandin F2alpha (5 x 10(-7) M), the arterioles within brain slices were evaluated using computer-assisted microscopy. Potassium chloride (KCl) induced vasodilation in cerebral arterioles from normotensive (5-10 mM) and hypertensive (5-15 mM) rats, whereas an inward rectifier K+ channel antagonist barium chloride (BaCl2; 10(-5) M) completely abolished the vasodilation in both strains. In arterioles of hypertensive rats, vasodilator responses to KCl were augmented compared with those in normotensive rats. In contrast, the vasodilator responses induced by sodium nitroprusside (3 x 10(-8) to 3 x 10(-6) M) in these two strains were similar. These results suggest that in cerebral cortex parenchymal microvessels, inward rectifier K+ channels play a crucial role in vasodilation produced by extracellular K+ and that the dilation of cerebral arterioles via these channels is augmented in chronic hypertension.
authors.affiliation: Department of Anesthesiology, Wakayama Medical University, Wakayama, Japan.
authors.forename: Katsutoshi
authors.initials: K
authors.lastname: Nakahata
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kinoshita
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Tokinaga
authors.forename: Yuko
authors.initials: Y
authors.lastname: Ishida
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Kimoto
authors.forename: Mayuko
authors.initials: M
authors.lastname: Dojo
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Mizumoto
authors.forename: Koji
authors.initials: K
authors.lastname: Ogawa
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Hatano
mesh_terms: D000818:Animals; D001160:Arterioles / Q000033:anatomy & histology / Q000502:physiology; D017609:Barium Compounds / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D001921:Brain / Q000098:blood supply*; D002560:Cerebrovascular Circulation; D002712:Chlorides / Q000494:pharmacology; D015237:Dinoprost / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D024661:Potassium Channels, Inwardly Rectifying / Q000037:antagonists & inhibitors / Q000502:physiology*; D011189:Potassium Chloride / Q000494:pharmacology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
chemical_list: D017609:Barium Compounds; D002712:Chlorides; D024661:Potassium Channels, Inwardly Rectifying; D014662:Vasoconstrictor Agents; C024986:barium chloride; D009599:Nitroprusside; D011189:Potassium Chloride; D015237:Dinoprost