extracellular calcium-dependent modulation of endothelium relaxation in rat mesenteric small artery: the role of potassium signaling

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ID: 215632
2015
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Abstract
The nature of NO- and COX-independent endothelial hyperpolarization (EDH) is not fully understood but activation of small- and intermittent-conductance Ca2+-activated K+ channels (SKCa and IKCa) is important. Previous studies have suggested that the significance of IKCa depends on Ca2+out. Also it has been suggested that K+ is important through localized K+out signaling causing activation of the Na+,K+-ATPase and inward-rectifying K+ channels (Kir). Here we tested the hypothesis that the modulating effect of Ca2+out on the EDH-like response depends on K+out. We addressed this possibility using isometric myography of rat mesenteric small arteries. When K+out was 4.2 mM, relaxation to acetylcholine (ACh) was stronger at 2.5 mM Ca2+out than at 1 mM Ca2+out. Inhibition of IKCa with TRAM34 suppressed the relaxations but did not change the relation between the relaxations at the low and high Ca2+out. This Ca2+out-dependence disappeared at 5.9 mM K+out and in the presence of ouabain or BaCl2. Our results suggest that IKCa are involved in the localized K+out signaling which acts through the Na+,K+-ATPase and Kir channels and that the significance of this endothelium-dependent pathway is modulated by Ca2+out.
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hangaard2015biomedextracellular Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Lise Hangaard;Peter B. Jessen;Dmitrii Kamaev;Christian Aalkjaer;Vladimir V. Matchkov
Journal spectrochimica acta - part a: molecular and biomolecular spectroscopy
Year 2015
DOI
10.1155/2015/758346
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