{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T02:24:22Z","timestamp":1790907862564,"version":"4.1.0"},"reference-count":37,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2001,6]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014Increased  endothelin-1 may be associated with elevation of blood pressure (BP)  and promotion of vascular hypertrophy, especially in  salt-sensitive hypertension. Mineralocorticoid hypertension has been  associated with activation of the endothelin system. We evaluated  whether in aldosterone-infused rats the selective  endothelin type A receptor-antagonist BMS 182874 prevents  BP elevation and vascular hypertrophy. Rats were infused  with aldosterone (0.75 \u03bcg\/h) subcutaneously via a  mini-osmotic pump and were offered 1% NaCl in the drinking water\u00b1BMS  182874 (40 mg\/kg in food) for 6 weeks. Systolic BP was  monitored by the tail-cuff method, and vascular changes of mesenteric  arteries were evaluated using a pressurized myograph.  Aldosterone-infusion significantly increased BP to  151\u00b17 mm Hg compared with controls (108\u00b14 mm Hg,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01). BMS 182874 normalized  BP (117\u00b14 mm Hg). Media cross-sectional area of aorta was  significantly increased by aldosterone infusion  (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05), and BMS treatment  normalized it (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.001).  Aldosterone infusion increased media width and  media-to-lumen ratio of mesenteric resistance arteries (17.6\u00b10.4 \u03bcm  and 7.5\u00b10.4%) compared with controls (14.2\u00b10.5 \u03bcm,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01, and 5.9\u00b10.1%,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). BMS 182874 normalized  media and media-to-lumen ratio (15.1\u00b10.6 \u03bcm and 5.7\u00b10.1%, both\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01). In conclusion, the  endothelin type A receptor antagonist attenuated BP  elevation and prevented vascular remodeling or hypertrophy  of aorta and mesenteric resistance arteries in  aldosterone-infused rats. These results suggest a role for  endothelin-1 in BP elevation and structural alterations of large and  small vessels in aldosterone and salt-induced  hypertension.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.37.6.1444","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"1444-1449","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":91,"title":["ET\n            <sub>A<\/sub>\n            Receptor Antagonist Prevents Blood Pressure Elevation and Vascular Remodeling in Aldosterone-Infused Rats"],"prefix":"10.1161","volume":"37","author":[{"given":"Jeong Bae","family":"Park","sequence":"first","affiliation":[{"name":"From the Clinical Research Institute of Montreal, University of Montreal  (J.B.P., E.L.S.), Montreal, Quebec, Canada; and Samsung Cheil Hospital,  Sungkyunkwan University School of Medicine (J.B.P.), Seoul, Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ernesto L.","family":"Schiffrin","sequence":"additional","affiliation":[{"name":"From the Clinical Research Institute of Montreal, University of Montreal  (J.B.P., E.L.S.), Montreal, Quebec, Canada; and Samsung Cheil Hospital,  Sungkyunkwan University School of Medicine (J.B.P.), Seoul, Korea."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"crossref","unstructured":"Schiffrin EL. 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