Endothelial dysfunction: its role in hypertensive coronary disease
PURPOSE OF REVIEWCoronary artery disease is the major cause of death worldwide. Hypertension is a major risk factor for developing coronary disease. It is now recognized that endothelial dysfunction is an early marker of coronary artery disease before structural changes to the vessel wall are appare...
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Veröffentlicht in: | Current opinion in cardiology 2005-07, Vol.20 (4), p.270-274 |
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description | PURPOSE OF REVIEWCoronary artery disease is the major cause of death worldwide. Hypertension is a major risk factor for developing coronary disease. It is now recognized that endothelial dysfunction is an early marker of coronary artery disease before structural changes to the vessel wall are apparent on angiography or intravascular ultrasound and that it has a prognostic value in predicting cardiovascular events in hypertensive patients. This review addresses recent developments in hypertension-induced endothelial dysfunction.
RECENT FINDINGSHyperaldosteronism causes endothelial dysfunction independent of high blood pressure. Exaggerated exercise blood pressure response has been related to endothelial dysfunction. Cyclosporin-A-induced endothelial dysfunction is related to reduced cholesterol content in caveolae. Chronic kidney disease induces changes in caveoli-1 and thus contributes to the reduced nitric oxide bioavailability, and causes oxidative stress independent of the high blood pressure. Asymmetric dimethylarginine plays a role in endothelial dysfunction in hypertensive patients independent of insulin resistance. 20-Hydroxyeicosatetraenoic acid is an independent predictor of hypertension in postmenopausal women. Endothelial dysfunction precedes and predicts the development of hypertension in postmenopausal women. Oral treatment with L-arginine improves endothelial dysfunction in hypertensives and lowers the blood pressure.
SUMMARYThe pathophysiology of endothelial dysfunction in hypertension is multifactorial. Recent findings have contributed to our understanding of mechanisms of endothelial dysfunction and support a role for early intervention to prevent irreversible vascular and organ damage. |
doi_str_mv | 10.1097/01.hco.0000167719.37700.1d |
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RECENT FINDINGSHyperaldosteronism causes endothelial dysfunction independent of high blood pressure. Exaggerated exercise blood pressure response has been related to endothelial dysfunction. Cyclosporin-A-induced endothelial dysfunction is related to reduced cholesterol content in caveolae. Chronic kidney disease induces changes in caveoli-1 and thus contributes to the reduced nitric oxide bioavailability, and causes oxidative stress independent of the high blood pressure. Asymmetric dimethylarginine plays a role in endothelial dysfunction in hypertensive patients independent of insulin resistance. 20-Hydroxyeicosatetraenoic acid is an independent predictor of hypertension in postmenopausal women. Endothelial dysfunction precedes and predicts the development of hypertension in postmenopausal women. Oral treatment with L-arginine improves endothelial dysfunction in hypertensives and lowers the blood pressure.
SUMMARYThe pathophysiology of endothelial dysfunction in hypertension is multifactorial. Recent findings have contributed to our understanding of mechanisms of endothelial dysfunction and support a role for early intervention to prevent irreversible vascular and organ damage.</description><identifier>ISSN: 0268-4705</identifier><identifier>EISSN: 1531-7080</identifier><identifier>DOI: 10.1097/01.hco.0000167719.37700.1d</identifier><identifier>PMID: 15956822</identifier><language>eng</language><publisher>United States: Lippincott Williams & Wilkins, Inc</publisher><subject>Angiotensin II - metabolism ; Antihypertensive Agents - therapeutic use ; Arginine - analogs & derivatives ; Arginine - blood ; Coronary Disease - blood ; Coronary Disease - physiopathology ; Coronary Disease - urine ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - physiopathology ; Humans ; Hydroxyeicosatetraenoic Acids - urine ; Hypertension - drug therapy ; Hypertension - physiopathology ; Nitric Oxide - metabolism ; Oxidants - metabolism</subject><ispartof>Current opinion in cardiology, 2005-07, Vol.20 (4), p.270-274</ispartof><rights>2005 Lippincott Williams & Wilkins, Inc.</rights><rights>2005 Lippincott Williams & Wilkins. 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4697-6bdee376000c85e3f8dc8fd5d9012ac4f7482dee3c09f6faf4aab386b2768df43</citedby><cites>FETCH-LOGICAL-c4697-6bdee376000c85e3f8dc8fd5d9012ac4f7482dee3c09f6faf4aab386b2768df43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15956822$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bolad, Islam</creatorcontrib><creatorcontrib>Delafontaine, Patrice</creatorcontrib><title>Endothelial dysfunction: its role in hypertensive coronary disease</title><title>Current opinion in cardiology</title><addtitle>Curr Opin Cardiol</addtitle><description>PURPOSE OF REVIEWCoronary artery disease is the major cause of death worldwide. Hypertension is a major risk factor for developing coronary disease. It is now recognized that endothelial dysfunction is an early marker of coronary artery disease before structural changes to the vessel wall are apparent on angiography or intravascular ultrasound and that it has a prognostic value in predicting cardiovascular events in hypertensive patients. This review addresses recent developments in hypertension-induced endothelial dysfunction.
RECENT FINDINGSHyperaldosteronism causes endothelial dysfunction independent of high blood pressure. Exaggerated exercise blood pressure response has been related to endothelial dysfunction. Cyclosporin-A-induced endothelial dysfunction is related to reduced cholesterol content in caveolae. Chronic kidney disease induces changes in caveoli-1 and thus contributes to the reduced nitric oxide bioavailability, and causes oxidative stress independent of the high blood pressure. Asymmetric dimethylarginine plays a role in endothelial dysfunction in hypertensive patients independent of insulin resistance. 20-Hydroxyeicosatetraenoic acid is an independent predictor of hypertension in postmenopausal women. Endothelial dysfunction precedes and predicts the development of hypertension in postmenopausal women. Oral treatment with L-arginine improves endothelial dysfunction in hypertensives and lowers the blood pressure.
SUMMARYThe pathophysiology of endothelial dysfunction in hypertension is multifactorial. Recent findings have contributed to our understanding of mechanisms of endothelial dysfunction and support a role for early intervention to prevent irreversible vascular and organ damage.</description><subject>Angiotensin II - metabolism</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Arginine - analogs & derivatives</subject><subject>Arginine - blood</subject><subject>Coronary Disease - blood</subject><subject>Coronary Disease - physiopathology</subject><subject>Coronary Disease - urine</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Humans</subject><subject>Hydroxyeicosatetraenoic Acids - urine</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - physiopathology</subject><subject>Nitric Oxide - metabolism</subject><subject>Oxidants - metabolism</subject><issn>0268-4705</issn><issn>1531-7080</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkMFuGyEURVGVqHHS_kI16n6cB8wAk0WlxnKSSpGyadcIw6NDMxksGMfy3wfXVtyyQeLde3g6hHylMKfQyWug897GOZRDhZS0m3MpoQzdBzKjLae1BAVnZAZMqLqR0F6Qy5z_lDzrOvGRXNC2a4VibEZul6OLU49DMEPldtlvRjuFON5UYcpVigNWYaz63RrThGMOr1jZmOJo0q5yIaPJ-ImcezNk_Hy8r8ivu-XPxUP9-HT_Y_H9sbaN6GQtVg6RS1G2sKpF7pWzyrvWdUCZsY2XjWL7iIXOC298Y8yKK7FiUijnG35Fvh24683qBZ3FcUpm0OsUXso2Opqg_5-Mode_46vmjElKRQHcHAA2xZwT-vcuBb03q4HqYlafzOq_ZjV1pfzl399P1aPKEmgOgW0cJkz5edhsMekezTD1B2Qrec0AWihMqPdPkr8B_suIhQ</recordid><startdate>200507</startdate><enddate>200507</enddate><creator>Bolad, Islam</creator><creator>Delafontaine, Patrice</creator><general>Lippincott Williams & Wilkins, Inc</general><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>5PM</scope></search><sort><creationdate>200507</creationdate><title>Endothelial dysfunction: its role in hypertensive coronary disease</title><author>Bolad, Islam ; Delafontaine, Patrice</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4697-6bdee376000c85e3f8dc8fd5d9012ac4f7482dee3c09f6faf4aab386b2768df43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Angiotensin II - metabolism</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Arginine - analogs & derivatives</topic><topic>Arginine - blood</topic><topic>Coronary Disease - blood</topic><topic>Coronary Disease - physiopathology</topic><topic>Coronary Disease - urine</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Humans</topic><topic>Hydroxyeicosatetraenoic Acids - urine</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - physiopathology</topic><topic>Nitric Oxide - metabolism</topic><topic>Oxidants - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bolad, Islam</creatorcontrib><creatorcontrib>Delafontaine, Patrice</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Current opinion in cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bolad, Islam</au><au>Delafontaine, Patrice</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelial dysfunction: its role in hypertensive coronary disease</atitle><jtitle>Current opinion in cardiology</jtitle><addtitle>Curr Opin Cardiol</addtitle><date>2005-07</date><risdate>2005</risdate><volume>20</volume><issue>4</issue><spage>270</spage><epage>274</epage><pages>270-274</pages><issn>0268-4705</issn><eissn>1531-7080</eissn><abstract>PURPOSE OF REVIEWCoronary artery disease is the major cause of death worldwide. Hypertension is a major risk factor for developing coronary disease. It is now recognized that endothelial dysfunction is an early marker of coronary artery disease before structural changes to the vessel wall are apparent on angiography or intravascular ultrasound and that it has a prognostic value in predicting cardiovascular events in hypertensive patients. This review addresses recent developments in hypertension-induced endothelial dysfunction.
RECENT FINDINGSHyperaldosteronism causes endothelial dysfunction independent of high blood pressure. Exaggerated exercise blood pressure response has been related to endothelial dysfunction. Cyclosporin-A-induced endothelial dysfunction is related to reduced cholesterol content in caveolae. Chronic kidney disease induces changes in caveoli-1 and thus contributes to the reduced nitric oxide bioavailability, and causes oxidative stress independent of the high blood pressure. Asymmetric dimethylarginine plays a role in endothelial dysfunction in hypertensive patients independent of insulin resistance. 20-Hydroxyeicosatetraenoic acid is an independent predictor of hypertension in postmenopausal women. Endothelial dysfunction precedes and predicts the development of hypertension in postmenopausal women. Oral treatment with L-arginine improves endothelial dysfunction in hypertensives and lowers the blood pressure.
SUMMARYThe pathophysiology of endothelial dysfunction in hypertension is multifactorial. Recent findings have contributed to our understanding of mechanisms of endothelial dysfunction and support a role for early intervention to prevent irreversible vascular and organ damage.</abstract><cop>United States</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>15956822</pmid><doi>10.1097/01.hco.0000167719.37700.1d</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Angiotensin II - metabolism Antihypertensive Agents - therapeutic use Arginine - analogs & derivatives Arginine - blood Coronary Disease - blood Coronary Disease - physiopathology Coronary Disease - urine Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Endothelium, Vascular - physiopathology Humans Hydroxyeicosatetraenoic Acids - urine Hypertension - drug therapy Hypertension - physiopathology Nitric Oxide - metabolism Oxidants - metabolism |
title | Endothelial dysfunction: its role in hypertensive coronary disease |
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