{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T18:53:06Z","timestamp":1791053586345,"version":"4.1.0"},"reference-count":31,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2003,2,5]],"date-time":"2003-02-05T00:00:00Z","timestamp":1044403200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2003,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Endothelial dysfunction is a characteristic of, and may be pathogenic in, inflammatory cardiovascular diseases, including sepsis. The mechanism underlying inflammation\u2010induced endothelial dysfunction may be related to the expression and activity of inducible nitric oxide synthase (iNOS). This possibility was investigated in isolated resistance (mesenteric) and conduit (aorta) arteries taken from lipopolysaccharide (LPS)\u2010treated (12.5 mg\/kg i.v.) or saline\u2010treated iNOS knockout (KO) and wild\u2010type (WT) mice. LPS pretreatment (for 15 h, but not 4 h) profoundly suppressed responses to acetylcholine (ACh) and significantly reduced sensitivity to the NO donor spermine\u2010NONOate (SPER\u2010NO) in aorta and mesenteric arteries of WT mice. This effect was temporally associated with iNOS protein expression in both conduit and resistance arteries and with a 10\u2010fold increase in plasma NO\n                    <jats:sub>x<\/jats:sub>\n                    levels. In contrast, no elevation of plasma NO\n                    <jats:sub>x<\/jats:sub>\n                    was observed in LPS\u2010treated iNOS KO animals, and arteries dissected from these animals did not express iNOS or display hyporeactivity to ACh or SPER\u2010NO. The mechanism underlying this phenomenon may be suppression of eNOS expression, as observed in arteries of WT animals, that was absent in arteries of iNOS KO animals. These results clearly demonstrate that iNOS induction plays an integral role in mediation of the endothelial dysfunction associated with sepsis in both resistance and conduit arteries.\n                  <\/jats:p>","DOI":"10.1096\/fj.02-0668fje","type":"journal-article","created":{"date-parts":[[2003,3,28]],"date-time":"2003-03-28T21:03:22Z","timestamp":1048885402000},"page":"773-775","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":126,"title":["Protection against lipopolysaccharide\u2010induced endothelial dysfunction in resistance and conduit vasculature of iNOS knockout mice"],"prefix":"10.1096","volume":"17","author":[{"given":"Sharmila D.","family":"Chauhan","sequence":"first","affiliation":[{"name":"Clinical Pharmacology, Barts and The London Queen Mary's School of Medicine Charterhouse Square London EC1M 6BQ UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gloria","family":"Seggara","sequence":"additional","affiliation":[{"name":"Department of Physiology University of Valencia Valencia Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Phuong A.","family":"Vo","sequence":"additional","affiliation":[{"name":"Clinical Pharmacology, Barts and The London Queen Mary's School of Medicine Charterhouse Square London EC1M 6BQ UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raymond J.","family":"Macallister","sequence":"additional","affiliation":[{"name":"Centre for Clinical Pharmacology University College London 5 University Street London WC1E 6JJ UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adrian J.","family":"Hobbs","sequence":"additional","affiliation":[{"name":"Wolfson Institute for Biomedical Research University College London Gower Street London WC1 UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amrita","family":"Ahluwalia","sequence":"additional","affiliation":[{"name":"Clinical Pharmacology, Barts and The London Queen Mary's School of Medicine Charterhouse Square London EC1M 6BQ UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2003,2,5]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1991.tb12298.x"},{"key":"e_1_2_6_3_1","first-page":"H1038","article-title":"Loss of vascular responsiveness induced by endotoxin involves L\u2010 arginine pathway","volume":"259","author":"Julou\u2010Schaeffer G.","year":"1990","journal-title":"Am. 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