{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T17:44:32Z","timestamp":1778867072608,"version":"3.51.4"},"reference-count":37,"publisher":"SAGE Publications","issue":"7","license":[{"start":{"date-parts":[[2009,7,31]],"date-time":"2009-07-31T00:00:00Z","timestamp":1248998400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Toxicol Ind Health"],"published-print":{"date-parts":[[2009,8]]},"abstract":"<jats:p>\n                    Abnormalities in the production and\/or release of relaxing factors from the endothelium have been implicated in the development of hypertension in several animal models. Endothelium-dependent relaxation has been reported to be impaired in thoracic aorta in experimentally induced and genetically hypertensive rats. Present study has extented these observations to thoracic aorta of cadmium-hypertensive rats. The possible role of alterations in oxidant status was also studied. Hypertension was induced by the intraperitoneal administration of 1 mg\/kg\/day cadmium for 15 days. Mechanical responses produced by acetylcholine (ACh, 10\n                    <jats:sup>\u2014 9<\/jats:sup>\n                    \u201410\n                    <jats:sup>\u20144<\/jats:sup>\n                    M) and sodium nitroprusside (SNP, 10\n                    <jats:sup>\u201410<\/jats:sup>\n                    \u201410\n                    <jats:sup>\u2014 5<\/jats:sup>\n                    M) were studied on phenylephrine-precontracted thoracic aorta rings from control and cadmium-hypertensive rats. Serum nitric oxide (NO) and aortic malondialdehyde (MDA) levels were measured. ACh-induced relaxation was attenuated in aorta from cadmium-hypertensive rats, whereas relaxation responses to SNP did not differ significantly between the groups. Exposure of aortic rings to N\n                    <jats:sup>G<\/jats:sup>\n                    -nitro-L-arginine methyl ester (L-NAME, 10\n                    <jats:sup>\u20144<\/jats:sup>\n                    M) resulted in a significantly greater inhibition of relaxation response to ACh in aortic rings of cadmium-hypertensive rats as compared with control rats. Incubation with L-arginine (L-Arg, 10\n                    <jats:sup>\u20143<\/jats:sup>\n                    M) caused a similar reversal of the inhibition of ACh-induced relaxation by L-NAME in both groups. Serum NO levels were decreased and aortic MDA levels were increased in cadmium-treated rats as compared with control rats. However, the differences between the groups did not reach a statistical significance. These findings suggested that the reduction in endothelium-dependent relaxation may play a role in cadmium-induced hypertension as it was in many other hypertension models.\n                  <\/jats:p>","DOI":"10.1177\/0748233709106822","type":"journal-article","created":{"date-parts":[[2009,7,31]],"date-time":"2009-07-31T20:55:19Z","timestamp":1249073719000},"page":"447-453","source":"Crossref","is-referenced-by-count":30,"title":["Impairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats"],"prefix":"10.1177","volume":"25","author":[{"given":"O.","family":"G\u00f6kalp","sequence":"first","affiliation":[{"name":"Department of Pharmacology, School of Medicine, Dicle University, Diyarbakir, Turkey,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"\u00d6zdem","sequence":"additional","affiliation":[{"name":"Biochemistry Unit, Central Laboratory, School of Medicine, Akdeniz University, Antalya, 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