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Title of Journal: Eur J Appl Physiol

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Abbravation: European Journal of Applied Physiology

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Springer-Verlag

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10.1007/s10776-016-0304-5

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1439-6327

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KSuperscript+/Superscript potentiates hyperosm

Authors: Ine De Clerck JeanLouis Pannier Johan Van de Voorde
Publish Date: 2006/01/17
Volume: 96, Issue: 6, Pages: 679-685
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Abstract

Several regulatory mechanisms have been proposed for the exercise hyperemia in skeletal muscles Since different vasoactive factors might interact during the hyperemic response we investigated the influence of elevated K+ concentrations on hyperosmolarity HOinduced vasorelaxations Small gluteal rat arteries were isolated and mounted in an organ bath for isometric tension recording After precontraction with norepinephrine 20 S20 40 S40 or 60 mM S60 sucrose was added in control conditions 5 mM K+ K5 or in the presence of additional 3 K8 or 5 mM K10 K+ Removal of the endothelium and the addition of ouabain Ba2+ iberiotoxin or 18α glycyrrhetinic acid αGA were used to study the underlying mechanisms Sucrose evoked significant concentrationdependent vasorelaxations S20 1562±161 S40 2647±171 S60 4366±250 which were significantly increased on addition of 3 and 5 mM After removal of the endothelium and in the presence of 5×10−5 M αGA the influence of K+ was significantly blocked but not in the presence of 5×10−5 M ouabain The KIR channel inhibitor Ba2+ and BKCa channel inhibitor iberiotoxin totally abolished the potentiating effect We conclude that K+ significantly enhances the relaxing effect of HO in gluteal blood vessels We hypothesize that K+ may stimulate the endothelial KIR channels which elicits the release of a mediator of the BKCa channels This factor may be transferred through myoendothelial gapjunctions to the smooth muscle cells where modulation of the BKCa channels sensitizes the arteries for hyperosmolarityinduced relaxations

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