title: K(+)-induced dilation of a small renal artery: no role for inward rectifier K+ channels.
abstract: OBJECTIVE
  To investigate the mechanism of K(+)-induced vasodilation in a small artery from the kidney, with a particular emphasis on the role of inward rectifier K+ channels.
  
  
  METHODS
  Lumen diameter and isometric tension recordings have been made from rabbit renal arcuate artery using pressurised- and wire-myography respectively. In addition, conventional whole-cell and amphotericin-perforated patch whole-cell recordings have been made from single smooth muscle cells isolated from the vessel.
  
  
  RESULTS
  Arcuate arteries dilated when the extracellular K+ concentration was raised to 8-10 mM from either zero or a normal physiological level of about 6 mM. The effect was not endothelium-dependent. Application of 0.01-1 mM Ba2+ to block inward rectifier K+ channels had no significant effect on K(+)-induced vasodilation in the arcuate artery, but under the same experimental conditions K(+)-induced dilation of the rat posterior cerebral artery was abolished by Ba2+. In the presence of 60 mM extracellular K+, inward rectifier K(+)-current was detectable in some single smooth muscle cells isolated from arcuate arteries but on average the current density was low (-1.44 pA pF-1 at -60 mV). K(+)-induced vasodilation of the arcuate artery was abolished by 10 microM ouabain and the half-effective concentration of K+ which induced vasodilation was 0.9-1.5 mM.
  
  
  CONCLUSIONS
  The observations suggest that an increase in the extracellular K+ concentration (up to about 10 mM) dilates the rabbit renal arcuate artery and that the primary mechanism underlying the effect may be stimulation of Na(+)-K+ ATPase in the smooth muscle cell membrane. Inward rectifier K+ channels have a low average density in smooth muscle cells isolated from arcuate arteries and play no significant role in K(+)-induced vasodilation.
authors.affiliation: Department of Pharmacology, University of Leeds, UK.
authors.forename: H M
authors.initials: HM
authors.lastname: Prior
authors.forename: N
authors.initials: N
authors.lastname: Webster
authors.forename: K
authors.initials: K
authors.lastname: Quinn
authors.forename: D J
authors.initials: DJ
authors.lastname: Beech
authors.forename: M S
authors.initials: MS
authors.lastname: Yates
mesh_terms: D000818:Animals; D001464:Barium / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D010042:Ouabain / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000494:pharmacology*; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D011817:Rabbits; D051381:Rats; D017208:Rats, Wistar; D012077:Renal Artery / Q000187:drug effects* / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors; D014664:Vasodilation
chemical_list: D004791:Enzyme Inhibitors; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D001464:Barium; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium