{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T08:09:43Z","timestamp":1793261383430,"version":"4.5.0"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2006,3]]},"abstract":"<jats:p>\n            Hydrogen peroxide causes vascular contraction and relaxation and contributes to the pathogenesis of hypertension. We hypothesized that the contractile state of blood vessels governs whether H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            causes contraction or relaxation. Hydrogen peroxide (1 \u03bcmol\/L to 1 mmol\/L) concentration-dependently contracted thoracic aorta and vena cava from sham normotensive and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The maximal contraction to H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            was 3 times greater in DOCA aorta compared with sham aorta but unchanged in DOCA vena cava compared with sham vena cava. In prostaglandin F\n            <jats:sub>2\u03b1<\/jats:sub>\n            (20 \u03bcmol\/L)\u2013contracted aorta and vena cava from sham and DOCA rats, H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            (1 \u03bcmol\/L to 1 mmol\/L) induced a concentration-dependent relaxation that was impaired in DOCA aorta but not DOCA vena cava. In contrast, in KCl (30 mmol\/L)-contracted vessels, maximal H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            -induced contraction was enhanced 15-fold in sham aorta and 5-fold in DOCA aorta but only 2-fold in sham vena cava. Tetraethylammonium (10 mmol\/L), BAY K 8644 (100 nmol\/L), and ouabain (1 mmol\/L) all enhanced maximal aortic H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            -induced contraction, whereas only ouabain enhanced venous H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            -induced contraction. The removal of extracellular Ca\n            <jats:sup>2+<\/jats:sup>\n            reduced H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            -induced contraction in KCl-contracted aorta, whereas maximal venous H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            -induced contraction (under basal conditions) was unchanged. Our data suggest that differences in arterial and venous K\n            <jats:sup>+<\/jats:sup>\n            channel activity and extracellular Ca\n            <jats:sup>2+<\/jats:sup>\n            influx are responsible for differences in arterial and venous contraction to H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            . In DOCA-salt hypertension, arterial but not venous contraction to H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            is enhanced, and relaxation to H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            is reduced.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.0000201540.91234.8f","type":"journal-article","created":{"date-parts":[[2006,1,24]],"date-time":"2006-01-24T01:44:00Z","timestamp":1138067040000},"page":"482-487","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":35,"title":["Pleiotropic Effects of Hydrogen Peroxide in Arteries and Veins From Normotensive and Hypertensive Rats"],"prefix":"10.1161","volume":"47","author":[{"given":"Keshari","family":"Thakali","sequence":"first","affiliation":[{"name":"From the Department of Pharmacology and Toxicology, Michigan State University, East Lansing."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren","family":"Davenport","sequence":"additional","affiliation":[{"name":"From the Department of Pharmacology and Toxicology, Michigan State University, East Lansing."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory D.","family":"Fink","sequence":"additional","affiliation":[{"name":"From the Department of Pharmacology and Toxicology, Michigan State University, East Lansing."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephanie W.","family":"Watts","sequence":"additional","affiliation":[{"name":"From the Department of Pharmacology and Toxicology, Michigan State University, East Lansing."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"H2686","volume":"272","year":"1997","unstructured":"Jin N, Rhoades RA. 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