{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T12:07:54Z","timestamp":1791029274019,"version":"4.1.0"},"reference-count":25,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2009,2,2]],"date-time":"2009-02-02T00:00:00Z","timestamp":1233532800000},"content-version":"vor","delay-in-days":2558,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2002,2]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>Vitamin C may influence NO\u2010dependent relaxation independently of effects on oxidant stress.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We investigated effects of vitamin C (0.1\u2003\u2013\u200310\u2003mmol\u2003l<jats:sup>\u22121<\/jats:sup>) on relaxation of pre\u2010constricted rabbit aortic rings to acetylcholine (ACh), authentic NO and the NO\u2010donors glyceryl trinitrate (GTN), nitroprusside (NP) and <jats:italic>S<\/jats:italic>\u2010nitroso\u2010<jats:italic>N<\/jats:italic>\u2010acetyl\u2010penicillamine (SNAP). DETCA (2\u2003\u2013\u20036\u2003mmol\u2003l<jats:sup>\u22121<\/jats:sup>), a cell permeable inhibitor of endogenous Cu\u2010Zn superoxide dismutase (SOD) was used to increase intracellular superoxide anion (O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Vitamin C reduced the response to ACh (71\u00b17% inhibition of maximum relaxation at 10\u2003mmol\u2003l<jats:sup>\u22121<\/jats:sup>) and inhibited relaxation to authentic NO. Vitamin C inhibited relaxation to GTN but potentiated relaxations to NP and SNAP, causing a parallel shift to a lower concentration range of the log dose\u2010response curve by approximately one log unit at the highest dose.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Vitamin C increased the concentration of NO in bath solution (plus EDTA, 1.0\u2003mmol\u2003l<jats:sup>\u22121<\/jats:sup>) following the addition of SNAP from 53\u00b114 to 771\u00b1101\u2003nmol\u2003l<jats:sup>\u22121<\/jats:sup> over the range 0.1\u2003\u2013\u20033.0\u2003mmol\u2003l<jats:sup>\u22121<\/jats:sup>.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>DETCA inhibited relaxation to ACh (71\u00b19% inhibition of maximum relaxation). This inhibition was abolished by a cell permeable SOD mimetic, but not by vitamin C. DETCA inhibited relaxation to SNAP but not that to NP nor to GTN.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Vitamin C inhibits endothelium\u2010dependent relaxations of rabbit aortic rings to ACh and authentic NO and does not reverse impaired relaxation resulting from increased intracellular oxidant stress. Vitamin C potentiates relaxation to the NO\u2010donors NP and SNAP by a mechanism that could involve release of NO from nitrosothiols.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2002) <jats:bold>135<\/jats:bold>, 1044\u20131050; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0704541\">10.1038\/sj.bjp.0704541<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0704541","type":"journal-article","created":{"date-parts":[[2005,1,28]],"date-time":"2005-01-28T21:43:12Z","timestamp":1106948592000},"page":"1044-1050","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Divergent effects of vitamin C on relaxations of rabbit aortic rings to acetylcholine and NO\u2010donors"],"prefix":"10.1111","volume":"135","author":[{"given":"K de","family":"Saram","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K L","family":"McNeill","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S","family":"Khokher","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J M","family":"Ritter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P J","family":"Chowienczyk","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,2,2]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0701218"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(99)00259-4"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.87.10.840"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.99.9.1156"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(99)04410-4"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1007\/PL00005231"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.26.6.863"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9149(99)80327-0"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(17)33675-X"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.94.1.6"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1039\/a803983f"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.97.4.363"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.83.9.916"},{"key":"e_1_2_7_15_1","first-page":"1256","article-title":"Spontaneous liberation of nitric oxide cannot account for in vitro vascular relaxation by S\u2010nitrosothiols","volume":"255","author":"KOWALUK E.A.","year":"1990","journal-title":"J. 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