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BioMed Research International
Volume 2015 (2015), Article ID 758346, 11 pages
http://dx.doi.org/10.1155/2015/758346
Research Article

Extracellular Calcium-Dependent Modulation of Endothelium Relaxation in Rat Mesenteric Small Artery: The Role of Potassium Signaling

1MEMBRANES, Department of Biomedicine, Health, Aarhus University, 8000 Aarhus, Denmark
2Department of Biomedicine, University of Copenhagen, Copenhagen, Denmark

Received 5 June 2015; Revised 11 August 2015; Accepted 16 August 2015

Academic Editor: Richardt G. Landgraf

Copyright © 2015 Lise Hangaard et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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 ( and ) is important. Previous studies have suggested that the significance of depends on . Also it has been suggested that K+ is important through localized signaling causing activation of the Na+,K+-ATPase and inward-rectifying K+ channels (). Here we tested the hypothesis that the modulating effect of on the EDH-like response depends on . We addressed this possibility using isometric myography of rat mesenteric small arteries. When was 4.2 mM, relaxation to acetylcholine (ACh) was stronger at 2.5 mM than at 1 mM . Inhibition of with TRAM34 suppressed the relaxations but did not change the relation between the relaxations at the low and high . This -dependence disappeared at 5.9 mM and in the presence of ouabain or BaCl2. Our results suggest that are involved in the localized signaling which acts through the Na+,K+-ATPase and channels and that the significance of this endothelium-dependent pathway is modulated by .