title: Hyperosmolarity increases K+-induced vasodilations in rat skeletal muscle arterioles.
abstract: OBJECTIVE
  Exercise hyperemia is mediated by a multitude of vasoactive metabolites released from the active skeletal muscle. Because several vasoactive factors might interact during the hyperemia response, we investigated the influence of hyperosmolarity (HO) on K(+)-induced relaxations.
  
  
  METHODS
  Small gluteal rat arteries (diameter: 245 +/- 6 microm) were isolated and mounted in an organ bath for isometric tension recording. After precontraction with norepinephrine, 1, 2, or 3 mM K(+) was added in both control, moderate, or high hyperosmotic (30 mM (S30) or 60 mM sucrose (S60)) conditions. Endothelial removal and the addition of ouabain, Ba(2+), 5-nitro-2-(3-phenyl-propylamino) benzoic acid (NPPB), or glibenclamide was used to study the underlying mechanisms.
  
  
  RESULTS
  The K(+)-induced relaxations were significantly (P < 0.001) increased in the presence of S30 and S60. Endothelial removal and the addition of glibenclamide or ouabain did not reduce the HO-induced increased sensitivity to K(+). The application of Ba abolished the influence of HO on the K(+)-induced relaxations. NPPB, a volume regulated anion channel (VRAC) blocker, mimicked the influence of HO by significantly (P < 0.05) increasing the K(+)-induced relaxations. Remarkably, the application of Ba(2+) abolished the sensitizing effect of NPPB on K(+)-induced relaxations.
  
  
  CONCLUSIONS
  HO increases the sensitivity of the rat gluteal skeletal muscle arteries to the vasodilating effect of K(+). It is hypothesized that HO inhibits VRAC causing smooth muscle hyperpolarization. This possibly sensitizes the K(ir)-channels that are known to be involved in the K-induced relaxations in this type of arteries.
authors.affiliation: Department of Movement and Sports Sciences, Ghent University, De Pintelaan 185, 9000 Ghent, Belgium.
authors.forename: Ine
authors.initials: I
authors.lastname: de Clerck
authors.forename: Koen
authors.initials: K
authors.lastname: Boussery
authors.forename: Jean-Louis
authors.initials: JL
authors.lastname: Pannier
authors.forename: Johan
authors.initials: J
authors.lastname: Van De Voorde
mesh_terms: D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D005260:Female; D006940:Hyperemia / Q000503:physiopathology; D007537:Isometric Contraction / Q000187:drug effects; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000503:physiopathology*; D009638:Norepinephrine / Q000494:pharmacology; D009994:Osmolar Concentration; D011188:Potassium / Q000494:pharmacology*; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects*; D050994:Voltage-Dependent Anion Channels / Q000187:drug effects
chemical_list: D015221:Potassium Channels; D014662:Vasoconstrictor Agents; D050994:Voltage-Dependent Anion Channels; D011188:Potassium; D009638:Norepinephrine