{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T16:57:23Z","timestamp":1761843443836},"reference-count":26,"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":[[2005,9]]},"abstract":"<jats:p>\n            The angiotensin II type 2 (AT\n            <jats:sub>2<\/jats:sub>\n            ) receptor is upregulated in pathological conditions such as vascular injury and exerts antagonistic effects against AT\n            <jats:sub>1<\/jats:sub>\n            receptor\u2013mediated actions. We examined the possibility that the sex difference in vascular remodeling is associated with altered AT\n            <jats:sub>2<\/jats:sub>\n            receptor expression, which is located on the X chromosome. In this study, we examined this possibility by using AT\n            <jats:sub>2<\/jats:sub>\n            receptor\u2013null (\n            <jats:italic>Agtr2\u2212<\/jats:italic>\n            ) mice. Vascular injury was induced by polyethylene cuff placement around the femoral artery of wild-type (\n            <jats:italic>Agtr2+<\/jats:italic>\n            ) and\n            <jats:italic>Agtr2\u2212<\/jats:italic>\n            mice. In\n            <jats:italic>Agtr2+<\/jats:italic>\n            mice, AT\n            <jats:sub>2<\/jats:sub>\n            receptor expression in the injured artery was enhanced, and this increase was greater in female than in male mice, with no significant difference in AT\n            <jats:sub>1<\/jats:sub>\n            receptor expression between male and female mice. Increases in neointimal formation, DNA synthesis, expression of monocyte chemoattractant protein-1, production of superoxide anion, and NADPH oxidase activity in the injured artery were attenuated in female compared with male mice. These parameters were augmented in\n            <jats:italic>Agtr2\u2212<\/jats:italic>\n            mice, whereas the sex differences in these parameters were smaller in\n            <jats:italic>Agtr2\u2212<\/jats:italic>\n            than in\n            <jats:italic>Agtr2+<\/jats:italic>\n            mice. Treatment with a nonhypotensive dose of the AT\n            <jats:sub>1<\/jats:sub>\n            receptor blocker valsartan decreased these parameters significantly in\n            <jats:italic>Agtr2+<\/jats:italic>\n            mice, and these inhibitory effects of valsartan were greater in female mice. This sex difference in valsartan\u2019s inhibitory effect was less marked in\n            <jats:italic>Agtr2\u2212<\/jats:italic>\n            mice. Our results suggest that the sex difference in response to vascular injury could be at least partially attributed to the exaggerated AT\n            <jats:sub>2<\/jats:sub>\n            receptor expression in the injured vessel in female mice.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.0000178564.14464.80","type":"journal-article","created":{"date-parts":[[2005,8,16]],"date-time":"2005-08-16T00:33:32Z","timestamp":1124152412000},"page":"577-583","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":51,"title":["Sex Difference in Vascular Injury and the Vasoprotective Effect of Valsartan Are Related to Differential AT\n            <sub>2<\/sub>\n            Receptor Expression"],"prefix":"10.1161","volume":"46","author":[{"given":"Midori","family":"Okumura","sequence":"first","affiliation":[{"name":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology (M.O., M.I., A.I., M.M., M.I., M.H.), and the Department of Obstetrics and Gynecology (M.O., M. Ito), Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masaru","family":"Iwai","sequence":"additional","affiliation":[{"name":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology (M.O., M.I., A.I., M.M., M.I., M.H.), and the Department of Obstetrics and Gynecology (M.O., M. Ito), Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ayumi","family":"Ide","sequence":"additional","affiliation":[{"name":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology (M.O., M.I., A.I., M.M., M.I., M.H.), and the Department of Obstetrics and Gynecology (M.O., M. Ito), Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masaki","family":"Mogi","sequence":"additional","affiliation":[{"name":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology (M.O., M.I., A.I., M.M., M.I., M.H.), and the Department of Obstetrics and Gynecology (M.O., M. Ito), Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masaharu","family":"Ito","sequence":"additional","affiliation":[{"name":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology (M.O., M.I., A.I., M.M., M.I., M.H.), and the Department of Obstetrics and Gynecology (M.O., M. Ito), Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masatsugu","family":"Horiuchi","sequence":"additional","affiliation":[{"name":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology (M.O., M.I., A.I., M.M., M.I., M.H.), and the Department of Obstetrics and Gynecology (M.O., M. Ito), Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.33.2.613"},{"key":"e_1_3_2_2_2","first-page":"415","volume":"52","year":"2000","unstructured":"de Gasparo M, Catt KJ, Inagami T, Wright TW, Unger T. International Union of Pharmacology, XXIII: the angiotensin II receptors. 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