Extracellular Calcium-Dependent Modulation of Endothelium Relaxation in Rat Mesenteric Small Artery: The Role of Potassium Signaling
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Extracellular Calcium-Dependent Modulation of Endothelium Relaxation in Rat Mesenteric Small Artery : The Role of Potassium Signaling. / Hangaard, Lise; Jessen, Peter B; Kamaev, Dmitrii; Aalkjaer, Christian; Matchkov, Vladimir V.
I: BioMed Research International, Bind 2015, 758346, 2015, s. 1-11.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Extracellular Calcium-Dependent Modulation of Endothelium Relaxation in Rat Mesenteric Small Artery
T2 - The Role of Potassium Signaling
AU - Hangaard, Lise
AU - Jessen, Peter B
AU - Kamaev, Dmitrii
AU - Aalkjaer, Christian
AU - Matchkov, Vladimir V
PY - 2015
Y1 - 2015
N2 - The nature of NO- and COX-independent endothelial hyperpolarization (EDH) is not fully understood but activation of small- and intermittent-conductance Ca(2+)-activated K(+) channels (SKCa and IKCa) is important. Previous studies have suggested that the significance of IKCa depends on [Ca(2+)]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 [Ca(2+)]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 [Ca(2+)]out than at 1 mM [Ca(2+)]out. Inhibition of IKCa with TRAM34 suppressed the relaxations but did not change the relation between the relaxations at the low and high [Ca(2+)]out. This [Ca(2+)]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 [Ca(2+)]out.
AB - The nature of NO- and COX-independent endothelial hyperpolarization (EDH) is not fully understood but activation of small- and intermittent-conductance Ca(2+)-activated K(+) channels (SKCa and IKCa) is important. Previous studies have suggested that the significance of IKCa depends on [Ca(2+)]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 [Ca(2+)]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 [Ca(2+)]out than at 1 mM [Ca(2+)]out. Inhibition of IKCa with TRAM34 suppressed the relaxations but did not change the relation between the relaxations at the low and high [Ca(2+)]out. This [Ca(2+)]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 [Ca(2+)]out.
U2 - 10.1155/2015/758346
DO - 10.1155/2015/758346
M3 - Journal article
C2 - 26504829
VL - 2015
SP - 1
EP - 11
JO - BioMed Research International
JF - BioMed Research International
SN - 2314-6133
M1 - 758346
ER -
ID: 154483108