{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T13:14:00Z","timestamp":1789910040198,"version":"4.0.1"},"reference-count":37,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2013,6,21]],"date-time":"2013-06-21T00:00:00Z","timestamp":1371772800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:list><jats:list-item><jats:p>Chronic intermittent hypoxia (<jats:styled-content style=\"fixed-case\">CIH<\/jats:styled-content>) contributes to the development of cardiovascular diseases in patients with obstructive sleep apnoea. Many studies have shown an association between increased circulating endothelin (<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>)\u20101 levels and<jats:styled-content style=\"fixed-case\">CIH<\/jats:styled-content>. The aim of the present study was to determine the role of<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>receptors in altered aortic function in an animal model of<jats:styled-content style=\"fixed-case\">CIH<\/jats:styled-content>.<\/jats:p><\/jats:list-item><jats:list-item><jats:p>Rats were subjected to<jats:styled-content style=\"fixed-case\">CIH<\/jats:styled-content>(<jats:italic>F<\/jats:italic><jats:sub>i<\/jats:sub><jats:sc>o<\/jats:sc><jats:sub>2<\/jats:sub>9% for 1\u00a0min, repeated every 2\u00a0min for 8\u00a0h\/day, 7\u00a0days\/week) for 3\u00a0weeks. After 3\u00a0weeks, the rats were killed and their aortas retrieved for use in<jats:italic>in vitro<\/jats:italic>experiments (isometric force measurement), histological analysis, immunohistochemistry and western blotting.<\/jats:p><\/jats:list-item><jats:list-item><jats:p>Aortas from rats subjected to<jats:styled-content style=\"fixed-case\">CIH<\/jats:styled-content>exhibited marked endothelial dysfunction and increased responsiveness to<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101. Furthermore,<jats:styled-content style=\"fixed-case\">CIH<\/jats:styled-content>induced increased<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 and<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content><jats:sub>A<\/jats:sub>receptor expression, whereas<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content><jats:sub>B<\/jats:sub>receptor expression was decreased. Aortic contractile responses to<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 were inhibited by the<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content><jats:sub>A<\/jats:sub>and<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content><jats:sub>B<\/jats:sub>receptor antagonists<jats:styled-content style=\"fixed-case\">BQ<\/jats:styled-content>\u2010123 and<jats:styled-content style=\"fixed-case\">BQ<\/jats:styled-content>\u2010788, respectively. Acetylcholine\u2010induced relaxation responses were significantly attenuated in aortas from rats subjected to<jats:styled-content style=\"fixed-case\">CIH<\/jats:styled-content>, whereas<jats:styled-content style=\"fixed-case\">CIH<\/jats:styled-content>had no significant effect on aortic responses to sodium nitroprusside.<\/jats:p><\/jats:list-item><jats:list-item><jats:p>The results of the present study suggest that increased expression of<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content><jats:sub>A<\/jats:sub>receptors, which mediate a potent vasoconstrictor response, plays an important role in the pathogenesis of<jats:styled-content style=\"fixed-case\">CIH<\/jats:styled-content>. In addition, decreased endothelial<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content><jats:sub>B<\/jats:sub>receptor expression, which is associated with the functional decline of endothelium\u2010dependent vasodilation, also contributes to the pathogenesis of<jats:styled-content style=\"fixed-case\">CIH<\/jats:styled-content>. It appears that the<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content><jats:sub>B<\/jats:sub>receptor\u2010induced buffering of<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 responsiveness is mediated via a nitric oxide\u2010dependent mechanism.<\/jats:p><\/jats:list-item><\/jats:list><\/jats:p>","DOI":"10.1111\/1440-1681.12109","type":"journal-article","created":{"date-parts":[[2013,5,11]],"date-time":"2013-05-11T11:12:43Z","timestamp":1368270763000},"page":"449-457","source":"Crossref","is-referenced-by-count":19,"title":["Endothelin receptors in augmented vasoconstrictor responses to endothelin\u20101 in chronic intermittent hypoxia"],"prefix":"10.1111","volume":"40","author":[{"given":"Qiu\u2010Hong","family":"Guo","sequence":"first","affiliation":[{"name":"Department of Pharmacology Hebei Medical University Shijiazhuang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi\u2010Long","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hebei Medical University Shijiazhuang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhuo","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hebei Medical University Shijiazhuang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ai\u2010Ying","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Biochemistry Hebei Medical University Shijiazhuang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi\u2010Hong","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Hebei Medical University Shijiazhuang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ya\u2010Jing","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hebei Medical University Shijiazhuang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J Woodrow","family":"Weiss","sequence":"additional","affiliation":[{"name":"Division of Pulmonary Critical Care and Sleep Medicine Beth Israel Deaconess Medical Center Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"En\u2010Sheng","family":"Ji","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hebei Medical University Shijiazhuang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Chu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Hebei Medical University Shijiazhuang China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,6,21]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200005113421901"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1997.00440360178019"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1378\/chest.123.1.244"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1164\/ajrccm.163.1.2001008"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.3109\/10623329709079869"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1159\/000050482"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2005.11.001"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.511"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1124\/pr.54.2.219"},{"key":"e_1_2_6_11_1","doi-asserted-by":"crossref","first-page":"137","DOI":"10.1016\/S0031-6997(25)06781-X","article-title":"International Union of Pharmacology nomenclature of endothelin receptors","volume":"46","author":"Masaki T","year":"1994","journal-title":"Pharmacol. 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