{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:30:43Z","timestamp":1771626643454,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2002,10,1]]},"abstract":"<jats:p>This study examined vascular function and the role of superoxide in mice that chronically express human renin (R+) and human angiotensinogen (A+). Responses of aortas from R+\/A+ mice and from their normotensive littermates (RA\u2212 mice) were examined in vitro. Endothelium-dependent relaxation to acetylcholine was impaired in vessels from R+\/A+ mice (e.g., maximal relaxation to 100 \u03bcM acetylcholine was 45 \u00b1 5% and 65 \u00b1 3% in R+\/A+ and RA\u2212 mice, respectively; P &lt; 0.05). Relaxation was also impaired to the endothelium-independent dilators authentic nitric oxide and nitroprusside in vessels from R+\/A+ mice. Maximal vasorelaxation to the endothelium-independent, non-nitric oxide dilator papaverine was similar in R+\/A+ and RA\u2212 mice. Incubation of vessels from R+\/A+ mice with Tiron (1 mM), a superoxide scavenger, improved relaxation to acetylcholine, nitric oxide, and nitroprusside. In contrast, incubation with diethyldithiocarbamate (1 mM), an inhibitor of copper-containing SODs, reduced acetylcholine- and nitroprusside-induced relaxation in vessels from both R+\/A+ and RA\u2212 mice. Basal superoxide levels, measured with lucigenin-enhanced chemiluminescence (5 \u03bcM lucigenin) and hydroethidine-based fluorescent confocal microscopy, were higher in vessels from R+\/A+ mice and were Tiron and polyethylene glycol-SOD sensitive. These results suggest that increased superoxide contributes to impaired nitric oxide-mediated relaxation in this genetic model of chronic angiotensin II-dependent hypertension.<\/jats:p>","DOI":"10.1152\/ajpheart.00079.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:04:03Z","timestamp":1425413043000},"page":"H1569-H1576","source":"Crossref","is-referenced-by-count":54,"title":["Superoxide contributes to vascular dysfunction in mice that express human renin and angiotensinogen"],"prefix":"10.1152","volume":"283","author":[{"given":"Sean P.","family":"Didion","sequence":"first","affiliation":[{"name":"Departments of Internal Medicine, Pathology, Physiology, and Pharmacology, Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa 52242"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael J.","family":"Ryan","sequence":"additional","affiliation":[{"name":"Departments of Internal Medicine, Pathology, 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