PMID- 14652495
OWN - NLM
STAT- MEDLINE
DCOM- 20040430
LR  - 20191210
IS  - 0195-9131 (Print)
IS  - 0195-9131 (Linking)
VI  - 35
IP  - 12
DP  - 2003 Dec
TI  - Potassium potently relaxes small rat skeletal muscle arteries.
PG  - 2005-12
AB  - INTRODUCTION: Skeletal muscle contraction elicits an explosive rise in 
      interstitial potassium (K+) concentration. K+ has been considered as one of the 
      most potent vasoactive metabolites in skeletal muscle arterioles. Studies on 
      isolated blood vessels report large relaxations when extracellular [K+] is 
      increased up to 10 mM. We studied the effects of smaller and physiologically more 
      relevant increases in [K+] (adding 1, 2, and 3 mM) and compared them with 
      relaxations induced by the endothelium derived hyperpolarizing factor (EDHF). 
      METHODS: Rat gluteal arteries were isolated and mounted in an organ bath for 
      isometric tension recording. After precontraction with norepinephrine, 
      acetylcholine or K+ was added in control conditions, after removal of the 
      endothelium or in the presence of ouabain or Ba2+. RESULTS: Application of 1, 2, 
      or 3 mM K+ induced large vasodilations (up to 75.4% with 3 mM) (N = 40), which 
      were more sustained at the higher concentrations. Removal of the vascular 
      endothelium had no effect on this relaxation. Inhibition of the Kir channels with 
      Ba2+ did not alter the K+-induced relaxations, although it significantly 
      inhibited the EDHF-mediated relaxation. Incubation with ouabain significantly 
      decreased the K+- and EDHF-induced relaxation. Simultaneous application of Ba2+ 
      and ouabain totally abolished both K+- and EDHF-induced responses. CONCLUSION: 
      Even small increases in extracellular K+ concentration elicit large 
      endothelium-independent and ouabain-sensitive relaxations in small skeletal 
      muscle arteries. The fact that both K+- and EDHF-induced vasorelaxations show 
      similar characteristics indicates that K+ might be the EDHF in this type of 
      artery.
FAU - De Clerck, Ine
AU  - De Clerck I
AD  - Department of Movement and Sports Sciences, Ghent University, Belgium.
FAU - Boussery, Koen
AU  - Boussery K
FAU - Pannier, Jean-Louis
AU  - Pannier JL
FAU - Van De Voorde, Johan
AU  - Van De Voorde J
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Med Sci Sports Exerc
JT  - Medicine and science in sports and exercise
JID - 8005433
RN  - 0 (Potassium Channels, Inwardly Rectifying)
RN  - EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Animals
MH  - Arteries/*drug effects
MH  - Drug Interactions
MH  - Female
MH  - Membrane Potentials/drug effects
MH  - Muscle Contraction/*drug effects/physiology
MH  - Muscle, Skeletal/*drug effects/physiology
MH  - Potassium/*pharmacology
MH  - Potassium Channels, Inwardly Rectifying
MH  - Rats
MH  - Rats, Wistar
MH  - *Sodium-Potassium-Exchanging ATPase
EDAT- 2003/12/04 05:00
MHDA- 2004/05/01 05:00
CRDT- 2003/12/04 05:00
PHST- 2003/12/04 05:00 [pubmed]
PHST- 2004/05/01 05:00 [medline]
PHST- 2003/12/04 05:00 [entrez]
AID - 10.1249/01.MSS.0000099101.39139.FA [doi]
PST - ppublish
SO  - Med Sci Sports Exerc. 2003 Dec;35(12):2005-12. doi: 
      10.1249/01.MSS.0000099101.39139.FA.