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Apart from the electrical propagation through myoendothelial gap junctions, the K<jats:sup>+<\/jats:sup> released from the endothelium facilitates <jats:styled-content style=\"fixed-case\">EDH<\/jats:styled-content> by increasing inward rectifier K<jats:sup>+<\/jats:sup> channel (Kir) conductance in smooth muscle cells. The <jats:styled-content style=\"fixed-case\">EDH<\/jats:styled-content>\u2010dependent relaxation of coronary artery (<jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>) and Kir current in smooth muscle cells (<jats:styled-content style=\"fixed-case\">CASMC<\/jats:styled-content>s) of hypertensive animals are poorly understood despite the critical role of coronary flow in the hypertrophic heart. In spontaneously hypertensive (<jats:styled-content style=\"fixed-case\">SHR<\/jats:styled-content>) and control (<jats:styled-content style=\"fixed-case\">WKY<\/jats:styled-content>) rats, we found attenuation of the <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content> relaxation by activators of <jats:styled-content style=\"fixed-case\">SK<\/jats:styled-content>3 and <jats:styled-content style=\"fixed-case\">SK<\/jats:styled-content>4 (<jats:styled-content style=\"fixed-case\">NS<\/jats:styled-content>309 and 1\u2010<jats:styled-content style=\"fixed-case\">EBIO<\/jats:styled-content>) in <jats:styled-content style=\"fixed-case\">SHR<\/jats:styled-content>. In isolated <jats:styled-content style=\"fixed-case\">CASMC<\/jats:styled-content>s, whole\u2010cell patch\u2010clamp study revealed larger <jats:italic>I<\/jats:italic><jats:sub>Kir<\/jats:sub> in <jats:styled-content style=\"fixed-case\">SHR<\/jats:styled-content> than <jats:styled-content style=\"fixed-case\">WKY<\/jats:styled-content>, whereas the myocytes of skeletal and cerebral arteries showed smaller <jats:italic>I<\/jats:italic><jats:sub>Kir<\/jats:sub> in <jats:styled-content style=\"fixed-case\">SHR<\/jats:styled-content> than <jats:styled-content style=\"fixed-case\">WKY<\/jats:styled-content>. While the treatment with <jats:italic>I<\/jats:italic><jats:sub>Kir<\/jats:sub> inhibitor (0.1\u00a0mmol\/L Ba<jats:sup>2+<\/jats:sup>) alone did not affect the <jats:styled-content style=\"fixed-case\">WKY<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>, the <jats:styled-content style=\"fixed-case\">SHR<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content> showed significant contractile response, suggesting relaxing influence of the higher <jats:styled-content style=\"fixed-case\"><jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub><\/jats:styled-content><jats:sub>ir<\/jats:sub> in the <jats:styled-content style=\"fixed-case\">CASMC<\/jats:styled-content>s of <jats:styled-content style=\"fixed-case\">SHR<\/jats:styled-content>. Furthermore, the attenuation of <jats:styled-content style=\"fixed-case\">NS<\/jats:styled-content>309\u2010induced relaxation of <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content> by the combined treatment with 0.1\u00a0mmol\/L Ba<jats:sup>2+<\/jats:sup> was more prominent in <jats:styled-content style=\"fixed-case\">SHR<\/jats:styled-content> than <jats:styled-content style=\"fixed-case\">WKY<\/jats:styled-content>. Our study firstly shows a distinct increase of <jats:styled-content style=\"fixed-case\"><jats:italic>I<\/jats:italic><jats:sub>K<\/jats:sub><\/jats:styled-content><jats:sub>ir<\/jats:sub> in the <jats:styled-content style=\"fixed-case\">CASMC<\/jats:styled-content>s of <jats:styled-content style=\"fixed-case\">SHR<\/jats:styled-content>, which could partly compensate for the attenuated relaxation via endothelial <jats:styled-content style=\"fixed-case\">SK<\/jats:styled-content>3 and <jats:styled-content style=\"fixed-case\">SK<\/jats:styled-content>4.<\/jats:p>","DOI":"10.1111\/1440-1681.13168","type":"journal-article","created":{"date-parts":[[2019,8,24]],"date-time":"2019-08-24T08:04:52Z","timestamp":1566633892000},"page":"38-48","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Increased inward rectifier K<sup>+<\/sup> current of coronary artery smooth muscle cells in spontaneously hypertensive rats; partial compensation of the attenuated endothelium\u2010dependent relaxation via Ca<sup>2+<\/sup>\u2010activated K<sup>+<\/sup> channels"],"prefix":"10.1111","volume":"47","author":[{"given":"Hae Jin","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Physiology Seoul National University College of Medicine Seoul Korea"},{"name":"Department of Biomedical Sciences Seoul National University College of Medicine Seoul Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming Zhe","family":"Yin","sequence":"additional","affiliation":[{"name":"Department of Physiology Seoul National University College of Medicine Seoul Korea"},{"name":"Department of Biomedical Sciences Seoul National University College of Medicine Seoul Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suhan","family":"Cho","sequence":"additional","affiliation":[{"name":"Department of Physiology Seoul National University College of Medicine Seoul Korea"},{"name":"Department 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