{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T10:17:10Z","timestamp":1790417830064,"version":"4.1.0"},"reference-count":24,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2009,1,30]],"date-time":"2009-01-30T00:00:00Z","timestamp":1233273600000},"content-version":"vor","delay-in-days":2131,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2003,4,1]],"date-time":"2003-04-01T00:00:00Z","timestamp":1049155200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2003,4]]},"abstract":"<jats:p>\n                    <jats:list list-type=\"explicit-label\">\n                      <jats:list-item>\n                        <jats:p>\n                          In this study, the role of endogenous H\n                          <jats:sub>2<\/jats:sub>\n                          O\n                          <jats:sub>2<\/jats:sub>\n                          as an endothelium\u2010dependent relaxant factor was characterised in aortas from C57BL\/6J and LDL receptor\u2010deficient mice (LDLR\n                          <jats:sup>\u2212\/\u2212<\/jats:sup>\n                          ).\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          Aortic rings from LDLR\n                          <jats:sup>\u2212\/\u2212<\/jats:sup>\n                          mice showed impaired endothelium\u2010dependent relaxation to acetylcholine (ACh; 0.001\u2013100\n                          <jats:italic>\u03bc<\/jats:italic>\n                          <jats:sc>M<\/jats:sc>\n                          ) and to the Ca\n                          <jats:sup>2+<\/jats:sup>\n                          ionophore A23187 (0.001\u20133\n                          <jats:italic>\u03bc<\/jats:italic>\n                          <jats:sc>M<\/jats:sc>\n                          ) compared with aortic rings from control mice. Endothelium\u2010independent relaxation produced by the NO donor, 3\u2010morpholino\u2010sydnonimine (SIN\u20101) was not different between strains.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          Pretreatment of vessels with\n                          <jats:sc>L<\/jats:sc>\n                          \u2010NNA (100\n                          <jats:italic>\u03bc<\/jats:italic>\n                          <jats:sc>M<\/jats:sc>\n                          ) or\n                          <jats:sc>L<\/jats:sc>\n                          \u2010NNA (100\n                          <jats:italic>\u03bc<\/jats:italic>\n                          <jats:sc>M<\/jats:sc>\n                          ) plus\n                          <jats:sc>L<\/jats:sc>\n                          \u2010NAME (300\n                          <jats:italic>\u03bc<\/jats:italic>\n                          <jats:sc>M<\/jats:sc>\n                          ) plus haemoglobin (10\n                          <jats:italic>\u03bc<\/jats:italic>\n                          <jats:sc>M<\/jats:sc>\n                          ) markedly decreased, but did not abolish the relaxation to ACh in control mice. In the aortas from LDLR\n                          <jats:sup>\u2212\/\u2212<\/jats:sup>\n                          mice treated with\n                          <jats:sc>L<\/jats:sc>\n                          \u2010NNA (100\n                          <jats:italic>\u03bc<\/jats:italic>\n                          <jats:sc>M<\/jats:sc>\n                          ), ACh induced a contractile effect. Catalase (800 and 2400 U ml\n                          <jats:sup>\u22121<\/jats:sup>\n                          ) shifted to the right the endothelium\u2010dependent relaxation to ACh in aortas from control but not from LDLR\n                          <jats:sup>\u2212\/\u2212<\/jats:sup>\n                          mice. Aminotriazole (50 m\n                          <jats:sc>M<\/jats:sc>\n                          ), which inhibits catalase, abolished its effect on control mice. Treatment of vessels with\n                          <jats:sc>L<\/jats:sc>\n                          \u2010NNA and catalase abolished vasorelaxation induced by ACh. Indomethacin (10\n                          <jats:italic>\u03bc<\/jats:italic>\n                          <jats:sc>M<\/jats:sc>\n                          ) did not modify the concentration\u2013response curve to ACh. Superoxide dismutase (300 U ml\n                          <jats:sup>\u22121<\/jats:sup>\n                          ) did not change ACh\u2010induced relaxation in both strains.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          Exogenous H\n                          <jats:sub>2<\/jats:sub>\n                          O\n                          <jats:sub>2<\/jats:sub>\n                          produced a concentration\u2010dependent relaxation in endothelium\u2010denuded aortic rings, which was not different between strains.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          It is concluded that H\n                          <jats:sub>2<\/jats:sub>\n                          O\n                          <jats:sub>2<\/jats:sub>\n                          greatly contributes to relaxation to ACh in aorta from control mice. Endothelial\u2010dependent relaxation to ACh is impaired in LDLR\n                          <jats:sup>\u2212\/\u2212<\/jats:sup>\n                          mice. Reduced biosynthesis or increased inactivation of H\n                          <jats:sub>2<\/jats:sub>\n                          O\n                          <jats:sub>2<\/jats:sub>\n                          is the possible mechanism responsible for endothelial dysfunction in aortas of atherosclerosis\u2010susceptible LDLR\n                          <jats:sup>\u2212\/\u2212<\/jats:sup>\n                          mice.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>British Journal of Pharmacology<\/jats:italic>\n                    (2003)\n                    <jats:bold>138<\/jats:bold>\n                    , 1215\u20131220. doi:\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0705164\">10.1038\/sj.bjp.0705164<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1038\/sj.bjp.0705164","type":"journal-article","created":{"date-parts":[[2003,4,23]],"date-time":"2003-04-23T16:34:36Z","timestamp":1051115676000},"page":"1215-1220","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["Endothelium dysfunction in LDL receptor knockout mice: a role for H\n                    <sub>2<\/sub>\n                    O\n                    <sub>2<\/sub>"],"prefix":"10.1111","volume":"138","author":[{"given":"Lu\u00edza A","family":"Rabelo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steyner F","family":"Cortes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacqueline I","family":"Alvarez\u2010Leite","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Virg\u00ednia S","family":"Lemos","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,1,30]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.279.2.H475"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.275.4.H1283"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(91)90935-Z"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1159\/000159147"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.99.13.1719"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.21.4.496"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.100.11.1230"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1970.50.3.319"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.21.6.1017"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.31.9.2224"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.10.4431"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200110056"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703705"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(99)00169-8"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1050-1738(01)00166-9"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1038\/35025203"},{"key":"e_1_2_7_18_1","doi-asserted-by":"publisher","DOI":"10.1042\/bj0680468"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2001.6278"},{"key":"e_1_2_7_20_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10506"},{"key":"e_1_2_7_21_1","doi-asserted-by":"crossref","first-page":"1205","DOI":"10.1016\/S0022-2275(20)33427-1","article-title":"Lipid peroxides induces expression of catalase in cultured vascular cells","volume":"41","author":"MEILHAC O.","year":"2000","journal-title":"J. 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