{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T16:47:13Z","timestamp":1783442833983,"version":"3.54.6"},"reference-count":33,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2021,4,20]],"date-time":"2021-04-20T00:00:00Z","timestamp":1618876800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2021,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Thromboxane A\n                      <jats:sub>2<\/jats:sub>\n                      (TXA\n                      <jats:sub>2<\/jats:sub>\n                      ) participates in many pathophysiological processes of coronary artery disease. However, its mechanism of TXA\n                      <jats:sub>2<\/jats:sub>\n                      \u2010induced contraction in the coronary artery remains to be clarified. A multi myograph system was used to measure the isometric tension of the mouse coronary arteries and identify the effect and pathway of TXA\n                      <jats:sub>2<\/jats:sub>\n                      analogues U46619. Confocal laser scanning microscopy was used to measure the intracellular calcium concentration ([Ca\n                      <jats:sup>2+<\/jats:sup>\n                      ]\n                      <jats:sub>i<\/jats:sub>\n                      ) in mouse coronary artery smooth muscle cells. Results from the experiment had shown that contraction in coronary artery was generated by U46619 in a concentration\u2010dependent manner, which was completely abolished by a specific TXA\n                      <jats:sub>2<\/jats:sub>\n                      receptor blocker, GR32191. PI\u2010PLC inhibitors U73122 and D609 and Rho\u2010Kinase inhibitor Y\u201027632 can block the U46619 elicited coronary artery contraction in a dose\u2010dependent manner. Then, the vasoconstriction response to U46619 was obviously inhibited by two pan\u2010PKC inhibitors chelerythrine or G\u04e76983, and a selective PKC\u03b4 inhibitor rottlerin, but was not blocked by a selective PKC\u03b6 inhibitor PKC\u2010PS or a selective PKC\u03b2 inhibitor hispidin. Meanwhile, the PKC activator PDBu\u2010induced vasoconstriction was significantly inhibited by 1\u00a0\u03bcmol\/L nifedipine, then mostly inhibited by 100\u00a0\u03bcmol\/L 2\u2010APB and 10\u00a0\u03bcmol\/L Y27632. We further found that the response to U46619 was inhibited, respectively, by three calcium channel blockers nifedipine, SKF96356 or 2\u2010APB in a concentration\u2010dependent manner. Although Store\u2010operated Ca\n                      <jats:sup>2+<\/jats:sup>\n                      (SOC) channels generated the increase of [Ca\n                      <jats:sup>2+<\/jats:sup>\n                      ]\n                      <jats:sub>i<\/jats:sub>\n                      in mouse coronary artery smooth muscle cells, SOC channels did not contribute to the vasoconstriction in mouse coronary arteries. Caffeine\u2010induced sarcoplasmic reticulum (SR) Ca\n                      <jats:sup>2+<\/jats:sup>\n                      release could obviously induce coronal vasoconstriction. In addition, NPPB, a cell membrane Ca\n                      <jats:sup>2+<\/jats:sup>\n                      activated C1\n                      <jats:sup>\u2212<\/jats:sup>\n                      channel blocker, could obviously inhibit the U46619\u2010induced vasoconstriction. The U46619\u2010induced mouse coronary artery contraction was involved in the increase in [Ca\n                      <jats:sup>2+<\/jats:sup>\n                      ]\n                      <jats:sub>i<\/jats:sub>\n                      mediated by Cav1.2, TRPC channels and SR release through the activation of G\u2010protein\u2010coupled TP receptors and the kinases signalling pathway in TP downstream proteins, while SOC channels did not participate in the vasoconstriction.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/1440-1681.13502","type":"journal-article","created":{"date-parts":[[2021,4,1]],"date-time":"2021-04-01T06:20:42Z","timestamp":1617258042000},"page":"996-1006","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Signalling pathway of U46619\u2010induced vascular smooth muscle contraction in mouse coronary artery"],"prefix":"10.1111","volume":"48","author":[{"given":"Run\u2010Sheng","family":"Jiang","sequence":"first","affiliation":[{"name":"Division of Cardiology Sun Yat\u2010sen Memorial Hospital Sun Yat\u2010sen University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3073-7738","authenticated-orcid":false,"given":"Li","family":"Zhang","sequence":"additional","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Clinical Pharmacology Research Center of Medical Sciences Guangdong Provincial People\u2019s Hospital Guangdong Academy of Medical Sciences Guangzhou China"},{"name":"School of Biological Science and Engineering South China University of Technology Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5283-1365","authenticated-orcid":false,"given":"Hui","family":"Yang","sequence":"additional","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Clinical Pharmacology Research Center of Medical Sciences Guangdong Provincial People\u2019s Hospital Guangdong Academy of Medical Sciences Guangzhou China"},{"name":"School of Biological Science and Engineering South China University of Technology Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8535-5123","authenticated-orcid":false,"given":"Meng\u2010Yuan","family":"Zhou","sequence":"additional","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Clinical Pharmacology Research Center of Medical Sciences Guangdong Provincial People\u2019s Hospital Guangdong Academy of Medical Sciences Guangzhou China"},{"name":"School of Biological Science and Engineering South China University of Technology Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chun\u2010Yu","family":"Deng","sequence":"additional","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Clinical 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