Role of Asymmetrical Dimethylarginine in Inflammation-Induced Endothelial Dysfunction in Human Atherosclerosis
We explored the role of asymmetrical dimethylarginine (ADMA) as a cause of endothelial dysfunction induced by systemic inflammation. In vitro data suggest that ADMA bioavailability is regulated by proinflammatory stimuli, but it is unclear whether ADMA is a link between inflammation and endothelial...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2011-07, Vol.58 (1), p.93-98 |
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| creator | Antoniades, Charalambos Demosthenous, Michael Tousoulis, Dimitris Antonopoulos, Alexios S Vlachopoulos, Charalambos Toutouza, Marina Marinou, Kyriakoula Bakogiannis, Constantinos Mavragani, Kleio Lazaros, George Koumallos, Nikolaos Triantafyllou, Costas Lymperiadis, Dimitris Koutsilieris, Michael Stefanadis, Christodoulos |
| description | We explored the role of asymmetrical dimethylarginine (ADMA) as a cause of endothelial dysfunction induced by systemic inflammation. In vitro data suggest that ADMA bioavailability is regulated by proinflammatory stimuli, but it is unclear whether ADMA is a link between inflammation and endothelial dysfunction in humans. In study 1 we recruited 351 patients with coronary artery disease (CAD) and 87 healthy controls. In study 2 we recruited 69 CAD, 69 healthy, and 10 patients with rheumatoid arthritis, whereas in study 3, 22 healthy and 70 CAD subjects were randomly assigned to Salmonella typhii vaccination (n=11 healthy and n=60 CAD) or placebo (n=11 healthy and n=10 CAD). Circulating interleukin 6/ADMA and flow-mediated dilation (FMD) were measured at 0 and 8 hours. In study 1, ADMA was inversely correlated with FMD in healthy individuals and CAD patients (P |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.110.168245 |
| format | Article |
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In vitro data suggest that ADMA bioavailability is regulated by proinflammatory stimuli, but it is unclear whether ADMA is a link between inflammation and endothelial dysfunction in humans. In study 1 we recruited 351 patients with coronary artery disease (CAD) and 87 healthy controls. In study 2 we recruited 69 CAD, 69 healthy, and 10 patients with rheumatoid arthritis, whereas in study 3, 22 healthy and 70 CAD subjects were randomly assigned to Salmonella typhii vaccination (n=11 healthy and n=60 CAD) or placebo (n=11 healthy and n=10 CAD). Circulating interleukin 6/ADMA and flow-mediated dilation (FMD) were measured at 0 and 8 hours. In study 1, ADMA was inversely correlated with FMD in healthy individuals and CAD patients (P<0.0001 for both). However, interleukin 6 was inversely correlated with FMD (P<0.0001) in healthy subjects but not in CAD patients. The positive correlation between ADMA and interleukin 6 was stronger in healthy (r=0.515; P<0.0001) compared with CAD (r=0.289; P=0.0001) subjects. In study 2, both patients with rheumatoid arthritis and CAD had higher interleukin 6 (P<0.0001) and ADMA (P=0.004) but lower FMD (P=0.001) versus healthy subjects. In study 3, vaccination increased interleukin 6 in healthy (P<0.001) and CAD (P<0.001) subjects. FMD was reduced in healthy subjects (P<0.05), but its reduction in CAD was borderline. Vaccination increased ADMA only in healthy subjects (P<0.001). Systemic, low-grade inflammation leads to increased ADMA that may induce endothelial dysfunction. This study demonstrated that ADMA may be a link between inflammation and endothelial dysfunction in humans.]]></description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.110.168245</identifier><identifier>PMID: 21518967</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Arginine - analogs & derivatives ; Arginine - blood ; Arterial hypertension. Arterial hypotension ; Atherosclerosis - blood ; Atherosclerosis - etiology ; Atherosclerosis - physiopathology ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Coronary Artery Disease - blood ; Coronary Artery Disease - etiology ; Coronary Artery Disease - physiopathology ; Disease Progression ; Endothelium, Vascular - physiopathology ; Experimental diseases ; Female ; Follow-Up Studies ; Humans ; Inflammation - blood ; Inflammation - complications ; Inflammation - physiopathology ; Male ; Medical sciences ; Pilot Projects ; Prognosis ; Vasodilation - physiology</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2011-07, Vol.58 (1), p.93-98</ispartof><rights>2011 American Heart Association, Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5115-4965742713c11bf64af06cb0347a46944706ff1eabe4dab89ac8a903ec6073473</citedby><cites>FETCH-LOGICAL-c5115-4965742713c11bf64af06cb0347a46944706ff1eabe4dab89ac8a903ec6073473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24258672$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21518967$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Antoniades, Charalambos</creatorcontrib><creatorcontrib>Demosthenous, Michael</creatorcontrib><creatorcontrib>Tousoulis, Dimitris</creatorcontrib><creatorcontrib>Antonopoulos, Alexios S</creatorcontrib><creatorcontrib>Vlachopoulos, Charalambos</creatorcontrib><creatorcontrib>Toutouza, Marina</creatorcontrib><creatorcontrib>Marinou, Kyriakoula</creatorcontrib><creatorcontrib>Bakogiannis, Constantinos</creatorcontrib><creatorcontrib>Mavragani, Kleio</creatorcontrib><creatorcontrib>Lazaros, George</creatorcontrib><creatorcontrib>Koumallos, Nikolaos</creatorcontrib><creatorcontrib>Triantafyllou, Costas</creatorcontrib><creatorcontrib>Lymperiadis, Dimitris</creatorcontrib><creatorcontrib>Koutsilieris, Michael</creatorcontrib><creatorcontrib>Stefanadis, Christodoulos</creatorcontrib><title>Role of Asymmetrical Dimethylarginine in Inflammation-Induced Endothelial Dysfunction in Human Atherosclerosis</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description><![CDATA[We explored the role of asymmetrical dimethylarginine (ADMA) as a cause of endothelial dysfunction induced by systemic inflammation. In vitro data suggest that ADMA bioavailability is regulated by proinflammatory stimuli, but it is unclear whether ADMA is a link between inflammation and endothelial dysfunction in humans. In study 1 we recruited 351 patients with coronary artery disease (CAD) and 87 healthy controls. In study 2 we recruited 69 CAD, 69 healthy, and 10 patients with rheumatoid arthritis, whereas in study 3, 22 healthy and 70 CAD subjects were randomly assigned to Salmonella typhii vaccination (n=11 healthy and n=60 CAD) or placebo (n=11 healthy and n=10 CAD). Circulating interleukin 6/ADMA and flow-mediated dilation (FMD) were measured at 0 and 8 hours. In study 1, ADMA was inversely correlated with FMD in healthy individuals and CAD patients (P<0.0001 for both). However, interleukin 6 was inversely correlated with FMD (P<0.0001) in healthy subjects but not in CAD patients. The positive correlation between ADMA and interleukin 6 was stronger in healthy (r=0.515; P<0.0001) compared with CAD (r=0.289; P=0.0001) subjects. In study 2, both patients with rheumatoid arthritis and CAD had higher interleukin 6 (P<0.0001) and ADMA (P=0.004) but lower FMD (P=0.001) versus healthy subjects. In study 3, vaccination increased interleukin 6 in healthy (P<0.001) and CAD (P<0.001) subjects. FMD was reduced in healthy subjects (P<0.05), but its reduction in CAD was borderline. Vaccination increased ADMA only in healthy subjects (P<0.001). Systemic, low-grade inflammation leads to increased ADMA that may induce endothelial dysfunction. This study demonstrated that ADMA may be a link between inflammation and endothelial dysfunction in humans.]]></description><subject>Arginine - analogs & derivatives</subject><subject>Arginine - blood</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Atherosclerosis - blood</subject><subject>Atherosclerosis - etiology</subject><subject>Atherosclerosis - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - etiology</subject><subject>Coronary Artery Disease - physiopathology</subject><subject>Disease Progression</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Experimental diseases</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Humans</subject><subject>Inflammation - blood</subject><subject>Inflammation - complications</subject><subject>Inflammation - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pilot Projects</subject><subject>Prognosis</subject><subject>Vasodilation - physiology</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkGGP1CAQhonReOvpXzCNifFTPYZSaP3WnKu7yeXOnGeinxpKwUUpPaHNZf_9Td09TY4EBuZ9hoGXkDdA3wMIONv8-LK-vllfft1eXTabBpMoiIrx8glZQcl4zktRPCUrCjXPa4DvJ-RFSr8oBc65fE5OGJRQ1UKuSLgevclGmzVpPwxmik4rn310uN3tvYo_XXDBZC5k22C9GgY1uTHk29DP2vTZOvTjtDPeLUX7ZOegF33hN_OgQtagGsek_bK69JI8s8on8-oYT8m3T-ub801-cfV5e95c5LoEKHNei1JyJqHQAJ0VXFkqdEcLLhUXNX6CCmvBqM7wXnVVrXSlaloYLahEqDgl7w733sbxz2zS1A4uaeO9CmacU1tJxjmVUCH54UBqfGCKxra30Q0q7lug7WJ3-8huTKLw124sfn1sM3eD6f-VPviLwNsjoBIaa6MK2qX_HGdlJSRDjh-4u9FPJqbffr4zsd0Z5addS3FwJqqcUWwu8ZTjhLK4B4bem5c</recordid><startdate>201107</startdate><enddate>201107</enddate><creator>Antoniades, Charalambos</creator><creator>Demosthenous, Michael</creator><creator>Tousoulis, Dimitris</creator><creator>Antonopoulos, Alexios S</creator><creator>Vlachopoulos, Charalambos</creator><creator>Toutouza, Marina</creator><creator>Marinou, Kyriakoula</creator><creator>Bakogiannis, Constantinos</creator><creator>Mavragani, Kleio</creator><creator>Lazaros, George</creator><creator>Koumallos, Nikolaos</creator><creator>Triantafyllou, Costas</creator><creator>Lymperiadis, Dimitris</creator><creator>Koutsilieris, Michael</creator><creator>Stefanadis, Christodoulos</creator><general>American Heart Association, Inc</general><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201107</creationdate><title>Role of Asymmetrical Dimethylarginine in Inflammation-Induced Endothelial Dysfunction in Human Atherosclerosis</title><author>Antoniades, Charalambos ; Demosthenous, Michael ; Tousoulis, Dimitris ; Antonopoulos, Alexios S ; Vlachopoulos, Charalambos ; Toutouza, Marina ; Marinou, Kyriakoula ; Bakogiannis, Constantinos ; Mavragani, Kleio ; Lazaros, George ; Koumallos, Nikolaos ; Triantafyllou, Costas ; Lymperiadis, Dimitris ; Koutsilieris, Michael ; Stefanadis, Christodoulos</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5115-4965742713c11bf64af06cb0347a46944706ff1eabe4dab89ac8a903ec6073473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Arginine - analogs & derivatives</topic><topic>Arginine - blood</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Atherosclerosis - blood</topic><topic>Atherosclerosis - etiology</topic><topic>Atherosclerosis - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - etiology</topic><topic>Coronary Artery Disease - physiopathology</topic><topic>Disease Progression</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Experimental diseases</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Humans</topic><topic>Inflammation - blood</topic><topic>Inflammation - complications</topic><topic>Inflammation - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pilot Projects</topic><topic>Prognosis</topic><topic>Vasodilation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Antoniades, Charalambos</creatorcontrib><creatorcontrib>Demosthenous, Michael</creatorcontrib><creatorcontrib>Tousoulis, Dimitris</creatorcontrib><creatorcontrib>Antonopoulos, Alexios S</creatorcontrib><creatorcontrib>Vlachopoulos, Charalambos</creatorcontrib><creatorcontrib>Toutouza, Marina</creatorcontrib><creatorcontrib>Marinou, Kyriakoula</creatorcontrib><creatorcontrib>Bakogiannis, Constantinos</creatorcontrib><creatorcontrib>Mavragani, Kleio</creatorcontrib><creatorcontrib>Lazaros, George</creatorcontrib><creatorcontrib>Koumallos, Nikolaos</creatorcontrib><creatorcontrib>Triantafyllou, Costas</creatorcontrib><creatorcontrib>Lymperiadis, Dimitris</creatorcontrib><creatorcontrib>Koutsilieris, Michael</creatorcontrib><creatorcontrib>Stefanadis, Christodoulos</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Antoniades, Charalambos</au><au>Demosthenous, Michael</au><au>Tousoulis, Dimitris</au><au>Antonopoulos, Alexios S</au><au>Vlachopoulos, Charalambos</au><au>Toutouza, Marina</au><au>Marinou, Kyriakoula</au><au>Bakogiannis, Constantinos</au><au>Mavragani, Kleio</au><au>Lazaros, George</au><au>Koumallos, Nikolaos</au><au>Triantafyllou, Costas</au><au>Lymperiadis, Dimitris</au><au>Koutsilieris, Michael</au><au>Stefanadis, Christodoulos</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Asymmetrical Dimethylarginine in Inflammation-Induced Endothelial Dysfunction in Human Atherosclerosis</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2011-07</date><risdate>2011</risdate><volume>58</volume><issue>1</issue><spage>93</spage><epage>98</epage><pages>93-98</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract><![CDATA[We explored the role of asymmetrical dimethylarginine (ADMA) as a cause of endothelial dysfunction induced by systemic inflammation. In vitro data suggest that ADMA bioavailability is regulated by proinflammatory stimuli, but it is unclear whether ADMA is a link between inflammation and endothelial dysfunction in humans. In study 1 we recruited 351 patients with coronary artery disease (CAD) and 87 healthy controls. In study 2 we recruited 69 CAD, 69 healthy, and 10 patients with rheumatoid arthritis, whereas in study 3, 22 healthy and 70 CAD subjects were randomly assigned to Salmonella typhii vaccination (n=11 healthy and n=60 CAD) or placebo (n=11 healthy and n=10 CAD). Circulating interleukin 6/ADMA and flow-mediated dilation (FMD) were measured at 0 and 8 hours. In study 1, ADMA was inversely correlated with FMD in healthy individuals and CAD patients (P<0.0001 for both). However, interleukin 6 was inversely correlated with FMD (P<0.0001) in healthy subjects but not in CAD patients. The positive correlation between ADMA and interleukin 6 was stronger in healthy (r=0.515; P<0.0001) compared with CAD (r=0.289; P=0.0001) subjects. In study 2, both patients with rheumatoid arthritis and CAD had higher interleukin 6 (P<0.0001) and ADMA (P=0.004) but lower FMD (P=0.001) versus healthy subjects. In study 3, vaccination increased interleukin 6 in healthy (P<0.001) and CAD (P<0.001) subjects. FMD was reduced in healthy subjects (P<0.05), but its reduction in CAD was borderline. Vaccination increased ADMA only in healthy subjects (P<0.001). Systemic, low-grade inflammation leads to increased ADMA that may induce endothelial dysfunction. This study demonstrated that ADMA may be a link between inflammation and endothelial dysfunction in humans.]]></abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>21518967</pmid><doi>10.1161/HYPERTENSIONAHA.110.168245</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Arginine - analogs & derivatives Arginine - blood Arterial hypertension. Arterial hypotension Atherosclerosis - blood Atherosclerosis - etiology Atherosclerosis - physiopathology Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Coronary Artery Disease - blood Coronary Artery Disease - etiology Coronary Artery Disease - physiopathology Disease Progression Endothelium, Vascular - physiopathology Experimental diseases Female Follow-Up Studies Humans Inflammation - blood Inflammation - complications Inflammation - physiopathology Male Medical sciences Pilot Projects Prognosis Vasodilation - physiology |
| title | Role of Asymmetrical Dimethylarginine in Inflammation-Induced Endothelial Dysfunction in Human Atherosclerosis |
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