title: Mechanism of extracellular K+-induced local and conducted responses in cerebral penetrating arterioles.
abstract: OBJECTIVE
  Extracellular concentration of potassium ion ([K+]o) may have a significant influence on the cerebral circulation in health and disease. Mechanisms of [K+]o-induced conducted vasomotor responses in cerebral arterioles, possibly linking microvascular regulation to neuronal activity, have not been examined.
  
  
  METHODS
  We analyzed vascular responses to small increases of [K+]o (up to 5 mmol/L) in isolated, cannulated, and pressurized rat cerebral arterioles (36.5+/-1.4 micro m). [K+]o was elevated globally through extraluminal application or locally through micropipette, while arteriolar diameter was measured online.
  
  
  RESULTS
  Elevation of [K+]o (5 mmol/L) produced dilation that was inhibited by ouabain but not BaCl2. Locally applied [K+]o (3 to 5 mmol/L) produced a biphasic response (initial constriction followed by dilation), both of which were conducted to the remote site (distance 1142+/-68 microm). Endothelial impairment inhibited conducted but not local biphasic responses. Extraluminal ouabain attenuated local and conducted secondary dilation but not initial constriction. The local biphasic response was unaffected by extraluminal or intraluminal BaCl2. Extraluminal but not intraluminal BaCl2 impaired both conducted constriction and dilation.
  
  
  CONCLUSIONS
  In rat penetrating arteriole, (1) [K+]o (3 to 5 mmol/L) strongly regulates arteriolar tone and causes conducted vasomotor responses; (2) local responses to elevated [K+]o are endothelium independent but conducted responses are dependent on an intact endothelium; (3) smooth muscle Na+-K+-ATPase activation is the generator of conducted dilation; and (4) smooth muscle inward rectifier potassium channels sustain conduction. Our findings suggest that potassium-induced conducted vasomotor responses may link local neuronal activity to microvascular regulation, which may be attenuated in pathological conditions.
authors.affiliation: Department of Neurosurgery, Washington University School of Medicine, St Louis, Mo 63110, USA.
authors.forename: Tetsuyoshi
authors.initials: T
authors.lastname: Horiuchi
authors.forename: Hans H
authors.initials: HH
authors.lastname: Dietrich
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Hongo
authors.forename: Ralph G
authors.initials: RG
authors.lastname: Dacey
mesh_terms: D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology; D001921:Brain / Q000098:blood supply*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004618:Embolism, Air / Q000503:physiopathology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism* / Q000494:pharmacology*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014654:Vascular Patency / Q000187:drug effects; D014666:Vasomotor System / Q000187:drug effects / Q000502:physiology
chemical_list: D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D026902:Potassium Channel Blockers; D010042:Ouabain; D019001:Nitric Oxide Synthase; D011188:Potassium