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      Inward rectifier potassium (Kir2.1) channels as end-stage boosters of endothelium-dependent vasodilators.

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          Abstract

          Increase in endothelial cell (EC) calcium activates calcium-sensitive intermediate and small conductance potassium (IK and SK) channels, thereby causing hyperpolarization and endothelium-dependent vasodilatation. Endothelial cells express inward rectifier potassium (Kir) channels, but their role in endothelium-dependent vasodilatation is not clear. In the mesenteric arteries, only ECs, but not smooth muscle cells, displayed Kir currents that were predominantly mediated by the Kir2.1 isoform. Endothelium-dependent vasodilatations in response to muscarinic receptor, TRPV4 (transient receptor potential vanilloid 4) channel and IK/SK channel agonists were highly attenuated by Kir channel inhibitors and by Kir2.1 channel knockdown. These results point to EC Kir channels as amplifiers of vasodilatation in response to increases in EC calcium and IK/SK channel activation and suggest that EC Kir channels could be targeted to treat endothelial dysfunction, which is a hallmark of vascular disorders.

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          Author and article information

          Journal
          J. Physiol. (Lond.)
          The Journal of physiology
          Wiley-Blackwell
          1469-7793
          0022-3751
          June 15 2016
          : 594
          : 12
          Affiliations
          [1 ] Department of Pharmacology, University of Vermont, VT, USA.
          [2 ] Department of Molecular Physiology and Biological Physics, University of Virginia, VA, USA.
          [3 ] Robert M. Berne Cardiovascular Research Center, University of Virginia, VA, USA.
          [4 ] Institute of Cardiovascular Sciences, University of Manchester, Manchester, UK.
          Article
          10.1113/JP271652
          4908010
          26840527

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