{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T23:01:17Z","timestamp":1789599677249,"version":"build-2803163510"},"reference-count":28,"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":[[2012,11]]},"abstract":"<jats:p>Prostaglandin E<jats:sub>2<\/jats:sub>is a major prostanoid found in the kidney and vasculature contributing to the regulation of blood pressure. The prostaglandin E<jats:sub>2<\/jats:sub>receptor EP1 has been shown to contribute to hypertension by mediating angiotensin II-dependent vasoconstriction, although its precise role is incompletely characterized. Disruption of the EP1 receptor in C57BL\/6J mice reduced the incidence of mortality during severe hypertension induced by uninephrectomy, deoxycorticosterone acetate, and angiotensin II. Mortality was dependent on all components of the model. Death was a result of aortic aneurysm rupture or occurred after development of anasarca, each of which was reduced in EP1\u2212\/\u2212 mice. Mean arterial pressure was increased in treated EP1+\/+ and EP1\u2212\/\u2212 mice; however, this elevation was significantly lower in EP1\u2212\/\u2212 mice. Blood pressure reduction via administration of hydralazine phenocopied EP1\u2212\/\u2212 mice. Thus, reduction in blood pressure by disruption of EP1 reduced incidence of mortality and decreased organ damage, suggesting that EP1 receptor blockade may be a viable target for antihypertensive therapy.<\/jats:p>","DOI":"10.1161\/hypertensionaha.112.199026","type":"journal-article","created":{"date-parts":[[2012,9,25]],"date-time":"2012-09-25T14:58:05Z","timestamp":1348585085000},"page":"1184-1191","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":17,"title":["EP1 Disruption Attenuates End-Organ Damage in a Mouse Model of Hypertension"],"prefix":"10.1161","volume":"60","author":[{"given":"Christina S.","family":"Bartlett","sequence":"first","affiliation":[{"name":"From the VA Tennessee Valley Healthcare System, Nashville, TN (R.C.H., R.Z., R.M.B.); Division of Nephrology and Hypertension, Department of Medicine (R.C.H., R.Z., R.M.B.), and Departments of Pharmacology (C.S.B., R.M.B.), and Pathology (K.L.B.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelli L.","family":"Boyd","sequence":"additional","affiliation":[{"name":"From the VA Tennessee Valley Healthcare System, Nashville, TN (R.C.H., R.Z., R.M.B.); Division of Nephrology and Hypertension, Department of Medicine (R.C.H., R.Z., R.M.B.), and Departments of Pharmacology (C.S.B., R.M.B.), and Pathology (K.L.B.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raymond C.","family":"Harris","sequence":"additional","affiliation":[{"name":"From the VA Tennessee Valley Healthcare System, Nashville, TN (R.C.H., R.Z., R.M.B.); Division of Nephrology and Hypertension, Department of Medicine (R.C.H., R.Z., R.M.B.), and Departments of Pharmacology (C.S.B., R.M.B.), and Pathology (K.L.B.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roy","family":"Zent","sequence":"additional","affiliation":[{"name":"From the VA Tennessee Valley Healthcare System, Nashville, TN (R.C.H., R.Z., R.M.B.); Division of Nephrology and Hypertension, Department of Medicine (R.C.H., R.Z., R.M.B.), and Departments of Pharmacology (C.S.B., R.M.B.), and Pathology (K.L.B.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard M.","family":"Breyer","sequence":"additional","affiliation":[{"name":"From the VA Tennessee Valley Healthcare System, Nashville, TN (R.C.H., R.Z., R.M.B.); Division of Nephrology and Hypertension, Department of Medicine (R.C.H., R.Z., R.M.B.), and Departments of Pharmacology (C.S.B., R.M.B.), and Pathology (K.L.B.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.18553\/jmcp.2007.13.s8-a.2"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/5583"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1021\/jm00197a012"},{"key":"e_1_3_4_5_2","first-page":"H449","article-title":"Prostaglandin E2-induced hypertension in conscious dogs.","volume":"237","author":"Hockel GM","year":"1979","unstructured":"Hockel GM, Cowley AW. 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