{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T14:42:53Z","timestamp":1761489773631,"version":"3.37.3"},"reference-count":37,"publisher":"Wiley","license":[{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"name":"Danish Research Council"},{"DOI":"10.13039\/501100004191","name":"Novo Nordisk","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004191","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100006197","name":"A.P. M\u00f8ller Foundation for the Advancement of Medical Science","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100006197","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["BioMed Research International"],"published-print":{"date-parts":[[2015]]},"abstract":"The nature of NO- and COX-independent endothelial hyperpolarization (EDH) is not fully understood but activation of small- and intermittent-conductance Ca2+<\/jats:sup>-activated K+<\/jats:sup>channels (SK<\/mml:mtext><\/mml:mrow>Ca<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>andIK<\/mml:mtext><\/mml:mrow>Ca<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>) is important. Previous studies have suggested that the significance ofIK<\/mml:mtext><\/mml:mrow>Ca<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>depends onCa<\/mml:mtext><\/mml:mrow>2<\/mml:mn>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>. Also it has been suggested that K+<\/jats:sup>is important through localizedK<\/mml:mtext><\/mml:mrow>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>signaling causing activation of the Na+<\/jats:sup>,K+<\/jats:sup>-ATPase and inward-rectifying K+<\/jats:sup>channels (K<\/mml:mtext><\/mml:mrow>ir<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>). Here we tested the hypothesis that the modulating effect ofCa<\/mml:mtext><\/mml:mrow>2<\/mml:mn>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>on the EDH-like response depends onK<\/mml:mtext><\/mml:mrow>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>. We addressed this possibility using isometric myography of rat mesenteric small arteries. WhenK<\/mml:mtext><\/mml:mrow>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>was 4.2\u2009mM, relaxation to acetylcholine (ACh) was stronger at 2.5\u2009mMCa<\/mml:mtext><\/mml:mrow>2<\/mml:mn>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>than at 1\u2009mMCa<\/mml:mtext><\/mml:mrow>2<\/mml:mn>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>. Inhibition ofIK<\/mml:mtext><\/mml:mrow>Ca<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>with TRAM34 suppressed the relaxations but did not change the relation between the relaxations at the low and highCa<\/mml:mtext><\/mml:mrow>2<\/mml:mn>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>. ThisCa<\/mml:mtext><\/mml:mrow>2<\/mml:mn>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>-dependence disappeared at 5.9\u2009mMK<\/mml:mtext><\/mml:mrow>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>and in the presence of ouabain or BaCl2<\/jats:sub>. Our results suggest thatIK<\/mml:mtext><\/mml:mrow>Ca<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>are involved in the localizedK<\/mml:mtext><\/mml:mrow>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>signaling which acts through the Na+<\/jats:sup>,K+<\/jats:sup>-ATPase andK<\/mml:mtext><\/mml:mrow>ir<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>channels and that the significance of this endothelium-dependent pathway is modulated byCa<\/mml:mtext><\/mml:mrow>2<\/mml:mn>+<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:mfenced><\/mml:mrow>out<\/mml:mtext><\/mml:mrow><\/mml:msub><\/mml:mrow><\/mml:math>.<\/jats:p>","DOI":"10.1155\/2015\/758346","type":"journal-article","created":{"date-parts":[[2015,10,4]],"date-time":"2015-10-04T17:06:05Z","timestamp":1443978365000},"page":"1-11","source":"Crossref","is-referenced-by-count":8,"title":["Extracellular 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