{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T04:26:42Z","timestamp":1792729602449,"version":"4.5.0"},"reference-count":57,"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":[[2016,5]]},"abstract":"<jats:p>\n            We investigated the role of angiotensin type 1a receptors (AGTR1a) in vascular injury induced by aldosterone activation of mineralocorticoid receptors in\n            <jats:italic>Agtr1a<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            and wild-type (WT) mice infused with aldosterone for 14 days while receiving 1% NaCl in drinking water. Aldosterone increased systolic blood pressure (BP) by \u224830 mm Hg in WT mice and \u224850 mm Hg in\n            <jats:italic>Agtr1a<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice. Aldosterone induced aortic and small artery remodeling, impaired endothelium-dependent relaxation in WT mice, and enhanced fibronectin and collagen deposition and vascular inflammation. None of these vascular effects were observed in\n            <jats:italic>Agtr1a<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice. Aldosterone effects were prevented by the AGTR1 antagonist losartan in WT mice. In contrast to aldosterone, norepinephrine caused similar BP increase and mesenteric artery remodeling in WT and\n            <jats:italic>Agtr1a<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice.\n            <jats:italic>Agtr1a<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice infused with aldosterone did not increase sodium excretion in response to a sodium chloride challenge, suggesting that sodium retention could contribute to the exaggerated BP rise induced by aldosterone.\n            <jats:italic>Agtr1a<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice had decreased mesenteric artery expression of the calcium-activated potassium channel\n            <jats:italic>Kcnmb1<\/jats:italic>\n            , which may enhance myogenic tone and together with sodium retention, exacerbate BP responses to aldosterone\/salt in\n            <jats:italic>Agtr1a<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice. We conclude that although aldosterone activation of mineralocorticoid receptors raises BP more in\n            <jats:italic>Agtr1a<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice, AGTR1a is required for mineralocorticoid receptor stimulation to induce vascular remodeling and inflammation and endothelial dysfunction.\n          <\/jats:p>","DOI":"10.1161\/hypertensionaha.115.07074","type":"journal-article","created":{"date-parts":[[2016,4,5]],"date-time":"2016-04-05T03:59:38Z","timestamp":1459828778000},"page":"897-905","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":58,"title":["Aldosterone-Induced Vascular Remodeling and Endothelial Dysfunction Require Functional Angiotensin Type 1a Receptors"],"prefix":"10.1161","volume":"67","author":[{"given":"Marie","family":"Briet","sequence":"first","affiliation":[{"name":"From the Lady Davis Institute for Medical Research (M.B., T.B., M.O.R.M., S.C.C., S.O., Y.R., P.P., E.L.S.) and Department of Medicine (M.B., E.L.S.), Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada; INSERM U1083, CNRS UMR 6214, Centre Hospitalo-Universitaire d\u2019Angers, Universit\u00e9 d\u2019Angers, Angers, France (M.B.); and Division of Nephrology, Department of Medicine, Duke University, Durham, NC (T.M.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tlili","family":"Barhoumi","sequence":"additional","affiliation":[{"name":"From the Lady Davis Institute for Medical Research (M.B., T.B., M.O.R.M., S.C.C., S.O., Y.R., P.P., E.L.S.) and Department of Medicine (M.B., E.L.S.), Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada; INSERM U1083, CNRS UMR 6214, Centre Hospitalo-Universitaire d\u2019Angers, Universit\u00e9 d\u2019Angers, Angers, France (M.B.); and Division of Nephrology, Department of Medicine, Duke University, Durham, NC (T.M.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muhammad Oneeb Rehman","family":"Mian","sequence":"additional","affiliation":[{"name":"From the Lady Davis Institute for Medical Research (M.B., T.B., M.O.R.M., S.C.C., S.O., Y.R., P.P., E.L.S.) and Department of Medicine (M.B., E.L.S.), Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada; INSERM U1083, CNRS UMR 6214, Centre Hospitalo-Universitaire d\u2019Angers, Universit\u00e9 d\u2019Angers, Angers, France (M.B.); and Division of Nephrology, Department of Medicine, Duke University, Durham, NC (T.M.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suellen C.","family":"Coelho","sequence":"additional","affiliation":[{"name":"From the Lady Davis Institute for Medical Research (M.B., T.B., M.O.R.M., S.C.C., S.O., Y.R., P.P., E.L.S.) and Department of Medicine (M.B., E.L.S.), Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada; INSERM U1083, CNRS UMR 6214, Centre Hospitalo-Universitaire d\u2019Angers, Universit\u00e9 d\u2019Angers, Angers, France (M.B.); and Division of Nephrology, Department of Medicine, Duke University, Durham, NC (T.M.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sofiane","family":"Ouerd","sequence":"additional","affiliation":[{"name":"From the Lady Davis Institute for Medical Research (M.B., T.B., M.O.R.M., S.C.C., S.O., Y.R., P.P., E.L.S.) and Department of Medicine (M.B., E.L.S.), Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada; INSERM U1083, CNRS UMR 6214, Centre Hospitalo-Universitaire d\u2019Angers, Universit\u00e9 d\u2019Angers, Angers, France (M.B.); and Division of Nephrology, Department of Medicine, Duke University, Durham, NC (T.M.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yohann","family":"Rautureau","sequence":"additional","affiliation":[{"name":"From the Lady Davis Institute for Medical Research (M.B., T.B., M.O.R.M., S.C.C., S.O., Y.R., P.P., E.L.S.) and Department of Medicine (M.B., E.L.S.), Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada; INSERM U1083, CNRS UMR 6214, Centre Hospitalo-Universitaire d\u2019Angers, Universit\u00e9 d\u2019Angers, Angers, France (M.B.); and Division of Nephrology, Department of Medicine, Duke University, Durham, NC (T.M.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas M.","family":"Coffman","sequence":"additional","affiliation":[{"name":"From the Lady Davis Institute for Medical Research (M.B., T.B., M.O.R.M., S.C.C., S.O., Y.R., P.P., E.L.S.) and Department of Medicine (M.B., E.L.S.), Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada; INSERM U1083, CNRS UMR 6214, Centre Hospitalo-Universitaire d\u2019Angers, Universit\u00e9 d\u2019Angers, Angers, France (M.B.); and Division of Nephrology, Department of Medicine, Duke University, Durham, NC (T.M.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierre","family":"Paradis","sequence":"additional","affiliation":[{"name":"From the Lady Davis Institute for Medical Research (M.B., T.B., M.O.R.M., S.C.C., S.O., Y.R., P.P., E.L.S.) and Department of Medicine (M.B., E.L.S.), Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada; INSERM U1083, CNRS UMR 6214, Centre Hospitalo-Universitaire d\u2019Angers, Universit\u00e9 d\u2019Angers, Angers, France (M.B.); and Division of Nephrology, Department of Medicine, Duke University, Durham, NC (T.M.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ernesto L.","family":"Schiffrin","sequence":"additional","affiliation":[{"name":"From the Lady Davis Institute for Medical Research (M.B., T.B., M.O.R.M., S.C.C., S.O., Y.R., P.P., E.L.S.) and Department of Medicine (M.B., E.L.S.), Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada; INSERM U1083, CNRS UMR 6214, Centre Hospitalo-Universitaire d\u2019Angers, Universit\u00e9 d\u2019Angers, Angers, France (M.B.); and Division of Nephrology, Department of Medicine, Duke University, Durham, NC (T.M.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2010.30"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1159\/000345243"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000034738.79310.06"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa030207"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199909023411001"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1177\/1470320309347785"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.8.3521"},{"issue":"4","key":"e_1_3_4_9_2","first-page":"F515","article-title":"Angiotensin II responses in AT1A receptor-deficient mice: a role for AT1B receptors in blood pressure regulation.","volume":"272","author":"Oliverio MI","year":"1997","unstructured":"Oliverio MI, Best CF, Kim HS, Arendshorst WJ, Smithies O, Coffman TM. 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