{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T20:38:31Z","timestamp":1791923911539,"version":"4.3.4"},"reference-count":25,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2001,11]]},"abstract":"<jats:p>\n            We previously reported increased aortic reactive oxygen species (ROS) production in mineralocorticoid (deoxycorticosterone acetate [DOCA]-salt) hypertensive rats. In the present study, we tested the hypothesis that NADH\/NADPH oxidase is responsible for increased ROS production, namely superoxide (O\n            <jats:sub>2<\/jats:sub>\n            <jats:sup>\u2212<\/jats:sup>\n            ), in aorta from the DOCA-salt rat. Treatment of aortic rings from DOCA-salt rats with the NO synthase inhibitor\n            <jats:italic>N<\/jats:italic>\n            -nitro-\n            <jats:sc>l<\/jats:sc>\n            -arginine and the xanthine oxidase inhibitor allopurinol did not significantly change O\n            <jats:sub>2<\/jats:sub>\n            <jats:sup>\u2212<\/jats:sup>\n            production. Furthermore, de-endothelialization of aorta from DOCA-salt rats did not affect O\n            <jats:sub>2<\/jats:sub>\n            <jats:sup>\u2212<\/jats:sup>\n            production compared with that of sham-operated rats. Thus, xanthine oxidase and uncoupled endothelial NO synthase were not responsible for increased O\n            <jats:sub>2<\/jats:sub>\n            <jats:sup>\u2212<\/jats:sup>\n            production in the DOCA-salt rats. In contrast, treatment with the NADPH oxidase inhibitor apocynin significantly decreased O\n            <jats:sub>2<\/jats:sub>\n            <jats:sup>\u2212<\/jats:sup>\n            production in aortic rings from DOCA-salt rats compared with sham-operated rats. Moreover, long-term administration of apocynin (in drinking water, 1.5 mmol\/L, 28 days) to DOCA-salt rats significantly decreased systolic blood pressure compared with that of rats treated with DOCA-salt alone. Furthermore, O\n            <jats:sub>2<\/jats:sub>\n            <jats:sup>\u2212<\/jats:sup>\n            production in aortic rings from DOCA-salt rats treated with apocynin for 28 days was reduced compared with that of untreated DOCA-salt rats. Reverse transcriptase\u2013polymerase chain reaction (RT-PCR) analysis demonstrated that DOCA-salt rats have significantly greater mRNA levels of the NADPH oxidase subunit p22phox than do sham-operated rats. These findings suggest that NADPH oxidase is increased and is responsible for increased O\n            <jats:sub>2<\/jats:sub>\n            <jats:sup>\u2212<\/jats:sup>\n            production and possibly contributes to increased blood pressure in the DOCA-salt hypertensive rat.\n          <\/jats:p>","DOI":"10.1161\/hy1101.093423","type":"journal-article","created":{"date-parts":[[2007,9,28]],"date-time":"2007-09-28T18:37:17Z","timestamp":1191004637000},"page":"1107-1111","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":258,"title":["NADH\/NADPH Oxidase and Enhanced Superoxide Production in the Mineralocorticoid Hypertensive Rat"],"prefix":"10.1161","volume":"38","author":[{"given":"Richard A.","family":"Beswick","sequence":"first","affiliation":[{"name":"From the Department of Physiology, Medical College of Georgia (A.M.D., R.C.W.), Augusta; Department of Physiology, University of Michigan (R.A.B.), Ann Arbor; and Department of Pharmacology, Federal University of Minas Gerais (R.L.), Belo Horizonte, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne M.","family":"Dorrance","sequence":"additional","affiliation":[{"name":"From the Department of Physiology, Medical College of Georgia (A.M.D., R.C.W.), Augusta; Department of Physiology, University of Michigan (R.A.B.), Ann Arbor; and Department of Pharmacology, Federal University of Minas Gerais (R.L.), Belo Horizonte, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Romulo","family":"Leite","sequence":"additional","affiliation":[{"name":"From the Department of Physiology, Medical College of Georgia (A.M.D., R.C.W.), Augusta; Department of Physiology, University of Michigan (R.A.B.), Ann Arbor; and Department of Pharmacology, Federal University of Minas Gerais (R.L.), Belo Horizonte, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. Clinton","family":"Webb","sequence":"additional","affiliation":[{"name":"From the Department of Physiology, Medical College of Georgia (A.M.D., R.C.W.), Augusta; Department of Physiology, University of Michigan (R.A.B.), Ann Arbor; and Department of Pharmacology, Federal University of Minas Gerais (R.L.), Belo Horizonte, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"155","volume":"24","year":"1995","unstructured":"Alexander RW. Hypertension and the pathogenesis of atherosclerosis: oxidative stress and the mediation of the arterial inflammatory response: a new perspective. Hypertension. 1995; 24: 155\u2013161.","journal-title":"Hypertension"},{"key":"e_1_3_2_2_2","first-page":"588","volume":"95","year":"1996","unstructured":"Rajagopalan S, Kurx S, Munzel T, Freemaan BA, Griendling KK, Harrison DG. 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Proc Natl Acad Sci U S A. 1998; 281: 627\u2013630.","journal-title":"Proc Natl Acad Sci U S A"},{"key":"e_1_3_2_9_2","first-page":"1201","volume":"134","year":"1989","unstructured":"Phan SH, Gannon DE, Varani J, Ryan US, Ward PA. Xanthine oxidase activity in rat pulmonary artery endothelial cells and its alteration by activated neutrophils. 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