{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T11:25:58Z","timestamp":1791199558443,"version":"4.2.0"},"reference-count":45,"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":[[2004,4]]},"abstract":"<jats:p>\n            Leukocyte adhesion to endothelial cells plays a key role in inflammatory processes associated with end-organ injury. Endothelin-1 (ET-1), which stimulates inflammatory processes, contributes to cardiovascular damage in deoxycorticosterone (DOCA)\u2013salt hypertension. We investigated whether ET\n            <jats:sub>A<\/jats:sub>\n            receptor blockade modulates in vivo leukocyte\u2013endothelial cell interactions and expression of cell adhesion molecules (CAM) involved in these processes. DOCA\u2013salt and control uninephrectomized rats were treated with the ET\n            <jats:sub>A<\/jats:sub>\n            antagonist BMS182874 (40 mg\/kg per day) or vehicle. Analysis of CAMs expression by reverse transcription-polymerase chain reaction and immunohistochemistry showed increased cardiac platelet selectin (P-selectin), detected mainly in endothelial cells, and vascular cell adhesion molecule-1 (VCAM-1), but not intercellular adhesion molecule-1 (ICAM-1), in DOCA\u2013salt rats. Cardiac expression of endothelial selectin (E-selectin) was decreased, whereas immunoreactivity to ED-1 and myeloperoxidase (MPO) activity, markers of macrophage and leukocyte infiltration, respectively, were increased in DOCA-salt. Leukocyte\u2013endothelial cell interaction, functionally assessed in venules of internal spermatic fascia by intravital microscopy, was significantly altered in DOCA\u2013salt rats as evidenced by increased leukocyte adhesion and decreased rolling. BMS182874 treatment normalized leukocyte\u2013endothelium interactions, decreased cardiac VCAM-1 expression in DOCA and control groups, and had no effects on ICAM-1 expression. BMS182874 also increased E-selectin and abolished P-selectin expression in DOCA-salt, but not in control rats. The ET\n            <jats:sub>A<\/jats:sub>\n            antagonist reduced cardiac ED-1 content and MPO activity and prevented cardiac damage in DOCA\u2013salt rats. These data indicate that ET-1 participates, via activation of ET\n            <jats:sub>A<\/jats:sub>\n            receptors, in altered leukocyte\u2013endothelial cell interactions in DOCA\u2013salt rats, possibly by modulating expression of CAMs, and that the inflammatory status is associated with cardiac damage in mineralocorticoid hypertension.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.0000117296.30296.14","type":"journal-article","created":{"date-parts":[[2004,3,2]],"date-time":"2004-03-02T01:56:29Z","timestamp":1078192589000},"page":"872-879","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":46,"title":["ET\n            <sub>A<\/sub>\n            Receptor Mediates Altered Leukocyte-Endothelial Cell Interaction and Adhesion Molecules Expression in DOCA\u2013Salt Rats"],"prefix":"10.1161","volume":"43","author":[{"given":"Glaucia E.","family":"Callera","sequence":"first","affiliation":[{"name":"From the Departments of Pharmacology (G.E.C., A.C.M., M.H.C.C., Z.B.F., D.N., R.C.T.) and Histology and Embryology (T.M.T.Z.), Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; and Clinical Research Institute of Montreal (G.E.C., R.M.T., E.L.S.), University of Montreal, Montreal, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Augusto C.","family":"Montezano","sequence":"additional","affiliation":[{"name":"From the Departments of Pharmacology (G.E.C., A.C.M., M.H.C.C., Z.B.F., D.N., R.C.T.) and Histology and Embryology (T.M.T.Z.), Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; and Clinical Research Institute of Montreal (G.E.C., R.M.T., E.L.S.), University of Montreal, Montreal, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rhian M.","family":"Touyz","sequence":"additional","affiliation":[{"name":"From the Departments of Pharmacology (G.E.C., A.C.M., M.H.C.C., Z.B.F., D.N., R.C.T.) and Histology and Embryology (T.M.T.Z.), Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; and Clinical Research Institute of Montreal (G.E.C., R.M.T., E.L.S.), University of Montreal, Montreal, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Telma M.T.","family":"Zorn","sequence":"additional","affiliation":[{"name":"From the Departments of Pharmacology (G.E.C., A.C.M., M.H.C.C., Z.B.F., D.N., R.C.T.) and Histology and Embryology (T.M.T.Z.), Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; and Clinical Research Institute of Montreal (G.E.C., R.M.T., E.L.S.), University of Montreal, Montreal, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Helena C.","family":"Carvalho","sequence":"additional","affiliation":[{"name":"From the Departments of Pharmacology (G.E.C., A.C.M., M.H.C.C., Z.B.F., D.N., R.C.T.) and Histology and Embryology (T.M.T.Z.), Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; and Clinical Research Institute of Montreal (G.E.C., R.M.T., E.L.S.), University of Montreal, Montreal, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zuleica B.","family":"Fortes","sequence":"additional","affiliation":[{"name":"From the Departments of Pharmacology (G.E.C., A.C.M., M.H.C.C., Z.B.F., D.N., R.C.T.) and Histology and Embryology (T.M.T.Z.), Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; and Clinical Research Institute of Montreal (G.E.C., R.M.T., E.L.S.), University of Montreal, Montreal, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dorothy","family":"Nigro","sequence":"additional","affiliation":[{"name":"From the Departments of Pharmacology (G.E.C., A.C.M., M.H.C.C., Z.B.F., D.N., R.C.T.) and Histology and Embryology (T.M.T.Z.), Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; and Clinical Research Institute of Montreal (G.E.C., R.M.T., E.L.S.), University of Montreal, Montreal, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ernesto L.","family":"Schiffrin","sequence":"additional","affiliation":[{"name":"From the Departments of Pharmacology (G.E.C., A.C.M., M.H.C.C., Z.B.F., D.N., R.C.T.) and Histology and Embryology (T.M.T.Z.), Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; and Clinical Research Institute of Montreal (G.E.C., R.M.T., E.L.S.), University of Montreal, Montreal, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rita C.","family":"Tostes","sequence":"additional","affiliation":[{"name":"From the Departments of Pharmacology (G.E.C., A.C.M., M.H.C.C., Z.B.F., D.N., R.C.T.) and Histology and Embryology (T.M.T.Z.), Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; and Clinical Research Institute of Montreal (G.E.C., R.M.T., E.L.S.), University of Montreal, Montreal, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.21.3.294"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.31.1.499"},{"key":"e_1_3_2_3_2","first-page":"1789.","volume":"10","year":"1999","unstructured":"Rothermund L, Yagil Y, Yagil C, Traupe T, Neumayer HH, Paul M, Kreutz R. 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