{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T06:16:42Z","timestamp":1780381002783,"version":"3.54.1"},"reference-count":37,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2013,3,12]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Recent studies have raised concern about the safety of erythropoiesis\u2010stimulating agents because of evidence of increased risk of hypertension and cardiovascular morbidity and mortality in chronic kidney disease (\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              ) patients. In the present study, we investigated the effects of recombinant human erythropoietin (\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              ) on endothelial function of gluteal subcutaneous resistance arteries isolated from 17 stage 4 patients (estimated glomerular filtration rate 21.9\u00b17.4\u00a0mL\/min per 1.73\u00a0m\n              <jats:sup>2<\/jats:sup>\n              ) aged 63\u00b113\u00a0years.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Arteries were mounted on a pressurized myograph.\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              impaired endothelium\u2010dependent relaxation in a concentration\u2010dependent manner. The maximal response to acetylcholine with\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              at 1, 10, and 20\u00a0IU\/mL was reduced by 12%, 34%, and 43%, respectively, compared with the absence of\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001).\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              \u2010induced endothelial dysfunction was significantly associated with carotid stiffness and history of cardiovascular events.\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              had no effect on norepinephrine\u2010induced vasoconstriction or sodium nitroprusside\u2013induced relaxation.\n              <jats:styled-content style=\"fixed-case\">ABT<\/jats:styled-content>\n              \u2010627, an endothelin type A receptor antagonist, and tempol, a superoxide dismutase mimetic, partially reversed the altered endothelial function in the presence of\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.01). Increased expression of endothelin\u20101 was found in the vessel wall after incubation with\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              .\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              alters endothelial function of resistance arteries in\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              patients via a mechanism involving in part oxidative stress and signaling through an endothelin type A receptor.\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              \u2010induced endothelial dysfunction could contribute to deleterious effects of\n              <jats:styled-content style=\"fixed-case\">EPO<\/jats:styled-content>\n              described in large interventional trials.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.113.000128","type":"journal-article","created":{"date-parts":[[2013,5,24]],"date-time":"2013-05-24T16:49:31Z","timestamp":1369414171000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":27,"title":["Effects of Recombinant Human Erythropoietin on Resistance Artery Endothelial Function in Stage 4 Chronic Kidney Disease"],"prefix":"10.1161","volume":"2","author":[{"given":"Marie","family":"Briet","sequence":"first","affiliation":[{"name":"Lady Davis Institute for Medical Research, Sir Mortimer B. Davis\u2010Jewish General Hospital, McGill University, Montreal, Quebec, Canada"},{"name":"Department of Medicine, Sir Mortimer B. Davis\u2010Jewish General Hospital, McGill University, Montreal, Quebec, Canada"},{"name":"Department of Pharmacology and Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale U970\u2010PARCC, H\u00f4pital Europ\u00e9en Georges Pompidou, Assistance Publique\u2010H\u00f4pitaux de Paris, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tlili","family":"Barhoumi","sequence":"additional","affiliation":[{"name":"Lady Davis Institute for Medical Research, Sir Mortimer B. Davis\u2010Jewish General Hospital, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muhammad Oneeb Rehman","family":"Mian","sequence":"additional","affiliation":[{"name":"Lady Davis Institute for Medical Research, Sir Mortimer B. Davis\u2010Jewish General Hospital, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristina","family":"Sierra","sequence":"additional","affiliation":[{"name":"Lady Davis Institute for Medical Research, Sir Mortimer B. Davis\u2010Jewish General Hospital, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierre","family":"Boutouyrie","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale U970\u2010PARCC, H\u00f4pital Europ\u00e9en Georges Pompidou, Assistance Publique\u2010H\u00f4pitaux de Paris, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Davidman","sequence":"additional","affiliation":[{"name":"Department of Medicine, Sir Mortimer B. Davis\u2010Jewish General Hospital, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Bercovitch","sequence":"additional","affiliation":[{"name":"Department of Medicine, Sir Mortimer B. Davis\u2010Jewish General Hospital, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sharon J.","family":"Nessim","sequence":"additional","affiliation":[{"name":"Department of Medicine, Sir Mortimer B. Davis\u2010Jewish General Hospital, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gershon","family":"Frisch","sequence":"additional","affiliation":[{"name":"Department of Medicine, Sir Mortimer B. 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