{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T18:51:14Z","timestamp":1782499874545,"version":"3.54.5"},"reference-count":28,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2005,10]]},"abstract":"<jats:p>\n            It is known that the endothelial function is compromised in atherosclerosis and arterial hypertension and that angiotensin is an important factor contributing to both pathophysiologies. The aim of this study was to evaluate the vascular function in a hypercholesterolemia\/atherosclerosis model, in the angiotensin II\u2013dependent 2-kidney 1-clip (2K1C) hypertension model and when both conditions coexist. Eight-week-old apolipoprotein E knockout (apoE; n=20) and C57BL\/6 (C57; n=20) mice underwent a 2K1C or sham operation and were studied 28 days later. Mean arterial pressure was higher in apoE\u20142K1C and C57\u20132K1C (126\u00b13 and 128\u00b13 mm Hg) when compared with the apoE\u2013Sham and C57\u2013Sham (103\u00b12 and 104\u00b12 mm Hg, respectively;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). The vascular reactivity to norepinephrine (NE; 10\n            <jats:sup>\u22129<\/jats:sup>\n            to 2\u00d710\n            <jats:sup>\u22123<\/jats:sup>\n            mol\/L), acetylcholine (ACh), and sodium nitroprusside (SNP; 10\n            <jats:sup>\u221210<\/jats:sup>\n            to 10\n            <jats:sup>\u22123<\/jats:sup>\n            mol\/L) was evaluated in the mesenteric arteriolar bed through concentration\u2013effect curves. NE caused vascular hyper-reactivity in apoE\u2013Sham, apoE\u20132K1C, and C57\u20132K1C (maximal response 146\u00b15, 144\u00b15, and 159\u00b14 mm Hg, respectively) compared with C57\u2013Sham (122\u00b17 mm Hg;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). The ACh-induced relaxation was smaller (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05) in apoE\u20132K1C and C57\u20132K1C (maximal response 53\u00b13% and 46\u00b13%) than in apoE\u2013Sham and C57\u2013Sham mice (78\u00b15% and 73\u00b14%). SNP-induced vascular relaxation showed similar concentration\u2013effect curves in all groups. We conclude that in C57\u20132K1C mice, the increased reactivity to NE and the decreased endothelium-dependent relaxation contribute to the maintenance of hypertension. The apoE mouse, at early stages of atherosclerosis, shows hyper-reactivity to NE but does not have endothelium dysfunction yet. However, the concurrence of both pathophysiologies does not result in additive effects on the vascular function.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.0000182154.61862.52","type":"journal-article","created":{"date-parts":[[2005,8,9]],"date-time":"2005-08-09T00:25:48Z","timestamp":1123547148000},"page":"932-936","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":44,"title":["Evaluation of Vascular Function in Apolipoprotein E Knockout Mice With Angiotensin-Dependent Renovascular Hypertension"],"prefix":"10.1161","volume":"46","author":[{"given":"Roberia M.P.","family":"Arruda","sequence":"first","affiliation":[{"name":"From the Laboratory of Transgenes and Cardiovascular Control (R.M.P.A., V.A.P. S.S.M., E.C.V.), Physiological Sciences Graduate Program, Biomedical Center, Federal University of Espirito Santo, Brazil; and College of Health Sciences of Vitoria (EMESCAM; E.C.V.), Vitoria, ES, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Veronica A.","family":"Peotta","sequence":"additional","affiliation":[{"name":"From the Laboratory of Transgenes and Cardiovascular Control (R.M.P.A., V.A.P. S.S.M., E.C.V.), Physiological Sciences Graduate Program, Biomedical Center, Federal University of Espirito Santo, Brazil; and College of Health Sciences of Vitoria (EMESCAM; E.C.V.), Vitoria, ES, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silvana S.","family":"Meyrelles","sequence":"additional","affiliation":[{"name":"From the Laboratory of Transgenes and Cardiovascular Control (R.M.P.A., V.A.P. S.S.M., E.C.V.), Physiological Sciences Graduate Program, Biomedical Center, Federal University of Espirito Santo, Brazil; and College of Health Sciences of Vitoria (EMESCAM; E.C.V.), Vitoria, ES, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisardo C.","family":"Vasquez","sequence":"additional","affiliation":[{"name":"From the Laboratory of Transgenes and Cardiovascular Control (R.M.P.A., V.A.P. S.S.M., E.C.V.), Physiological Sciences Graduate Program, Biomedical Center, Federal University of Espirito Santo, Brazil; and College of Health Sciences of Vitoria (EMESCAM; E.C.V.), Vitoria, ES, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/362801a0"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199901143400207"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.103.3.448"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(92)90362-G"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.10.4471"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.32.11.2658"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(01)00469-2"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(01)01140-2"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1159\/000070705"},{"key":"e_1_3_2_10_2","first-page":"50","volume":"13","year":"1992","unstructured":"Luscher TF. 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