{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T06:55:23Z","timestamp":1763535323976},"reference-count":35,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,3,27]],"date-time":"2015-03-27T00:00:00Z","timestamp":1427414400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"navy logistics scientific research subjects","award":["00-3321"],"award-info":[{"award-number":["00-3321"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2015,4]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>To provide pharmacological data for future clinical studies, this study investigated the protective effects of diltiazem on vascular endothelial cell (<jats:styled-content style=\"fixed-case\">VEC<\/jats:styled-content>) injury induced by angiotensin\u2010<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> (Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>), hypoxia, and a combination of both treatments. The concentration of intracellular free calcium and the mitochondrial membrane potential in <jats:styled-content style=\"fixed-case\">VEC<\/jats:styled-content> were assessed as indicators of cell injury. An <jats:italic>in vivo<\/jats:italic> hypoxic animal model was used to test the protective effect of diltiazem on vascular endothelial tissues. Our study showed that Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> and hypoxia decreased the mitochondrial membrane potential in <jats:styled-content style=\"fixed-case\">VEC<\/jats:styled-content>, which was significantly inhibited by diltiazem. Diltiazem protected against <jats:styled-content style=\"fixed-case\">VEC<\/jats:styled-content> injury induced by the increased concentration of intracellular free calcium, which was associated with Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> and hypoxia. Diltiazem reduced the apoptosis of rat <jats:styled-content style=\"fixed-case\">VEC<\/jats:styled-content> under a sustained hypoxic condition. In addition, it reduced Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> and endothelin I levels in rat vascular endothelial tissues. Our study confirmed that Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> and hypoxia induced <jats:styled-content style=\"fixed-case\">VEC<\/jats:styled-content> injury by regulating the levels of mitochondrial membrane potential and intracellular free calcium. Diltiazem, a calcium channel blocker, protected <jats:styled-content style=\"fixed-case\">VEC<\/jats:styled-content> from Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u2010 and hypoxia\u2010induced injury.<\/jats:p>","DOI":"10.1111\/1440-1681.12371","type":"journal-article","created":{"date-parts":[[2015,2,6]],"date-time":"2015-02-06T14:06:47Z","timestamp":1423231607000},"page":"337-343","source":"Crossref","is-referenced-by-count":5,"title":["Protective effects of diltiazem against vascular endothelial cell injury induced by angiotensin\u2010<scp>II<\/scp> and hypoxia"],"prefix":"10.1111","volume":"42","author":[{"given":"Minggao","family":"Li","sequence":"first","affiliation":[{"name":"Aviation and Diving Medical Center Navy General Hospital Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jing","family":"Li","sequence":"additional","affiliation":[{"name":"Aviation and Diving Medical Center Navy General Hospital Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guo","family":"Meng","sequence":"additional","affiliation":[{"name":"Aviation and Diving Medical Center Navy General Hospital Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xin","family":"Liu","sequence":"additional","affiliation":[{"name":"Aviation and Diving Medical Center Navy General Hospital Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2015,3,27]]},"reference":[{"key":"e_1_2_8_2_1","first-page":"3527","article-title":"Endothelial cells in physiology and in the pathophysiology of vascular disorders","volume":"91","author":"Cines DB","year":"1998","journal-title":"Blood"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2012.29"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/s12012-012-9184-9"},{"key":"e_1_2_8_5_1","first-page":"553","article-title":"Osteopontin is required for angiotensin II\u2010induced migration of vascular smooth muscle cells","volume":"67","author":"Qiu ZB","year":"2012","journal-title":"Pharmazie"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.185116"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1253\/circj.CJ-11-1507"},{"key":"e_1_2_8_8_1","doi-asserted-by":"crossref","first-page":"87","DOI":"10.3233\/CH-2012-1569","article-title":"Microcirculatory effects of angiotensin II inhibitors in patients with severe heart failure","volume":"54","author":"Salgado DR","year":"2012","journal-title":"Clin. 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