title: K+ as a vasodilator in resting human muscle: implications for exercise hyperaemia.
abstract: OBJECTIVE
  Potassium (K(+)) released from contracting skeletal muscle is considered a vasodilatory agent. This concept is mainly based on experiments infusing non-physiological doses of K(+). The aim of the present study was to investigate the role of K(+) in blood flow regulation.
  
  
  METHODS
  We measured leg blood flow (LBF) and arterio-venous (A-V) O(2) difference in 13 subjects while infusing K(+) into the femoral artery at a rate of 0.2, 0.4, 0.6 and 0.8 mmol min(-1).
  
  
  RESULTS
  The lowest dose increased the calculated femoral artery plasma K(+) concentration by approx.1 mmol L(-1). Graded K(+) infusions increased LBF from 0.39 +/- 0.06 to 0.56 +/- 0.13, 0.58 +/- 0.17, 0.61 +/- 0.11 and 0.71 +/- 0.17 L min(-1), respectively, whereas the leg A-V O(2) difference decreased from 74 +/- 9 to 60 +/- 12, 52 +/- 11, 53 +/- 9 and 45 +/- 7 mL L(-1), respectively (P < 0.05). Mean arterial pressure was unchanged, indicating that the increase in LBF was associated with vasodilatation. The effect of K(+) was totally inhibited by infusion (27 micromol min(-1)) of Ba(2+), an inhibitor of Kir2.1 channels. Simultaneous infusion of ATP and K(+) evoked an increase in LBF equalled to the sum of their effects.
  
  
  CONCLUSIONS
  Physiological infusions of K(+) induce significant increases in resting LBF, which are completely blunted by inhibition of the Kir2.1 channels. The present findings in resting skeletal muscle suggest that K(+) released from contracting muscle might be involved in exercise hyperaemia. However, the magnitude of increase in LBF observed with K(+) infusion suggests that K(+) only accounts for a limited fraction of the hyperaemic response to exercise.
authors: Institute of Molecular Biology and Physiology, Copenhagen Muscle Research Centre, University of Copenhagen, Copenhagen, Denmark. cjuel@aki.ku.dk
authors: C
authors: C
authors: Juel
authors: S
authors: S
authors: Olsen
authors: R L
authors: RL
authors: Rentsch
authors: J
authors: J
authors: González-Alonso
authors: J B
authors: JB
authors: Rosenmeier
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology; D000328:Adult; D001464:Barium / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D015444:Exercise / Q000502:physiology*; D005263:Femoral Artery / Q000502:physiology; D006801:Humans; D006940:Hyperemia / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000503:physiopathology; D011188:Potassium / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying / Q000037:antagonists & inhibitors / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D012146:Rest / Q000502:physiology; D014664:Vasodilation / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: C489457:KCNJ2 protein, human; D024661:Potassium Channels, Inwardly Rectifying; D014665:Vasodilator Agents; D001464:Barium; D000255:Adenosine Triphosphate; D011188:Potassium