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Visceral obesity is characterized by impaired nitric oxide-independent vasodilation
Background Endothelial dysfunction has been described in obesity. This study examines the impact of visceral obesity on nitric oxide-independent relaxation in the human forearm. Methods and results In ten viscerally obese and ten matched controls forearm blood flow (FBF) was measured by venous occlu...
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Published in: | European heart journal 2003-07, Vol.24 (13), p.1210-1215 |
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description | Background Endothelial dysfunction has been described in obesity. This study examines the impact of visceral obesity on nitric oxide-independent relaxation in the human forearm. Methods and results In ten viscerally obese and ten matched controls forearm blood flow (FBF) was measured by venous occlusion plethysmography during intrabrachial infusion of: (1) sodium nitroprusside; (2) bradykinin, before and after inhibition of vasoactive prostaglandins and nitric oxide; (3) potassium; (4) ouabain (Na+/K+ATPase inhibitor) alone or (5) in combination with BaCl2(KIRinhibitor). Baseline FBF and endothelium-independent vasodilatation were similar in the two groups. In obese patients, bradykinin-induced increase of FBF was significantly less than in controls (P |
doi_str_mv | 10.1016/S0195-668X(03)00206-9 |
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This study examines the impact of visceral obesity on nitric oxide-independent relaxation in the human forearm. Methods and results In ten viscerally obese and ten matched controls forearm blood flow (FBF) was measured by venous occlusion plethysmography during intrabrachial infusion of: (1) sodium nitroprusside; (2) bradykinin, before and after inhibition of vasoactive prostaglandins and nitric oxide; (3) potassium; (4) ouabain (Na+/K+ATPase inhibitor) alone or (5) in combination with BaCl2(KIRinhibitor). Baseline FBF and endothelium-independent vasodilatation were similar in the two groups. In obese patients, bradykinin-induced increase of FBF was significantly less than in controls (P<0.01). Irrespective of prostaglandins and nitric oxide inhibition, bradykinin response was lower in the viscerally obese. Intrabrachial potassium determined a significantly blunted response (P<0.05). Ouabain caused a similar, moderate decrease in basal FBF in the two groups; the coinfusion of BaCl2caused a more intense decline in FBF which was significantly relevant in obese (−24±5%, P<0.01). Conclusions In obese patients there is a blunted nitric oxide-independent relaxation determined by a decreased response of inwardly rectifying potassium channels.</description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1016/S0195-668X(03)00206-9</identifier><identifier>PMID: 12831815</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Barium Compounds - pharmacology ; Biological and medical sciences ; Brachial Artery ; Bradykinin - pharmacology ; Cardiology. Vascular system ; Chlorides - pharmacology ; Cyclooxygenase Inhibitors - pharmacology ; Dose-Response Relationship, Drug ; Endothelium ; Endothelium, Vascular ; Endothelium-derived hyperpolarizing factor ; Forearm - blood supply ; Humans ; Infusions, Intravenous ; Insulin resistance ; Male ; Medical sciences ; Nitric Oxide - physiology ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitroprusside - pharmacology ; Obesity ; Obesity - physiopathology ; Ouabain - pharmacology ; Plethysmography ; Potassium - pharmacology ; Potassium channels ; Vasodilation - drug effects ; Vasodilation - physiology ; Vasodilator Agents - pharmacology</subject><ispartof>European heart journal, 2003-07, Vol.24 (13), p.1210-1215</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-aef7acd3f12563d244a61cae5022f4e221e1910fc044cbd6492cbe6e7773e6173</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15625088$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12831815$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vigili de Kreutzenberg, S.</creatorcontrib><creatorcontrib>Kiwanuka, E.</creatorcontrib><creatorcontrib>Tiengo, A.</creatorcontrib><creatorcontrib>Avogaro, A.</creatorcontrib><title>Visceral obesity is characterized by impaired nitric oxide-independent vasodilation</title><title>European heart journal</title><addtitle>Eur Heart J</addtitle><description>Background Endothelial dysfunction has been described in obesity. This study examines the impact of visceral obesity on nitric oxide-independent relaxation in the human forearm. Methods and results In ten viscerally obese and ten matched controls forearm blood flow (FBF) was measured by venous occlusion plethysmography during intrabrachial infusion of: (1) sodium nitroprusside; (2) bradykinin, before and after inhibition of vasoactive prostaglandins and nitric oxide; (3) potassium; (4) ouabain (Na+/K+ATPase inhibitor) alone or (5) in combination with BaCl2(KIRinhibitor). Baseline FBF and endothelium-independent vasodilatation were similar in the two groups. In obese patients, bradykinin-induced increase of FBF was significantly less than in controls (P<0.01). Irrespective of prostaglandins and nitric oxide inhibition, bradykinin response was lower in the viscerally obese. Intrabrachial potassium determined a significantly blunted response (P<0.05). Ouabain caused a similar, moderate decrease in basal FBF in the two groups; the coinfusion of BaCl2caused a more intense decline in FBF which was significantly relevant in obese (−24±5%, P<0.01). Conclusions In obese patients there is a blunted nitric oxide-independent relaxation determined by a decreased response of inwardly rectifying potassium channels.</description><subject>Adult</subject><subject>Barium Compounds - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Brachial Artery</subject><subject>Bradykinin - pharmacology</subject><subject>Cardiology. Vascular system</subject><subject>Chlorides - pharmacology</subject><subject>Cyclooxygenase Inhibitors - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelium</subject><subject>Endothelium, Vascular</subject><subject>Endothelium-derived hyperpolarizing factor</subject><subject>Forearm - blood supply</subject><subject>Humans</subject><subject>Infusions, Intravenous</subject><subject>Insulin resistance</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitroprusside - pharmacology</subject><subject>Obesity</subject><subject>Obesity - physiopathology</subject><subject>Ouabain - pharmacology</subject><subject>Plethysmography</subject><subject>Potassium - pharmacology</subject><subject>Potassium channels</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNpFkEtv1EAMgEcIRLelPwGUC1U5BOx5JTlW5VHQqlWfqriMnIkjBrLJdiaLWn492e6qvdiW_XlG_oR4i_ARAe2nS8DK5NaWt4egPgBIsHn1QszQSJlXVpuXYvaE7IjdlH4DQGnRvhY7KEuFJZqZuLwJyXOkLhtqTmF8yELK_C-K5EeO4R83WT31FksKcar7MMbgs-E-NJyHvuElT6Efs7-UhiZ0NIahfyNetdQl3t_mPXH99cvV8Uk-P_v2_fhonnstYcyJ24J8o1qUxqpGak0WPbEBKVvNUiJjhdB60NrXjdWV9DVbLopCscVC7YmDzbvLONytOI1usT6m66jnYZVcoTRajXoCzQb0cUgpcuuWMSwoPjgEt7bpHm26tSoHyj3adNW09277wapecPO8tdU3Ae-3ACVPXRup9yE9c8ZKA2U5cfmGC2nk-6c5xT_OFqow7uT2pzvXPy4-z69O3YX6DxxHjeU</recordid><startdate>20030701</startdate><enddate>20030701</enddate><creator>Vigili de Kreutzenberg, S.</creator><creator>Kiwanuka, E.</creator><creator>Tiengo, A.</creator><creator>Avogaro, A.</creator><general>Oxford University Press</general><scope>BSCLL</scope><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>20030701</creationdate><title>Visceral obesity is characterized by impaired nitric oxide-independent vasodilation</title><author>Vigili de Kreutzenberg, S. ; Kiwanuka, E. ; Tiengo, A. ; Avogaro, A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-aef7acd3f12563d244a61cae5022f4e221e1910fc044cbd6492cbe6e7773e6173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adult</topic><topic>Barium Compounds - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Brachial Artery</topic><topic>Bradykinin - pharmacology</topic><topic>Cardiology. Vascular system</topic><topic>Chlorides - pharmacology</topic><topic>Cyclooxygenase Inhibitors - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelium</topic><topic>Endothelium, Vascular</topic><topic>Endothelium-derived hyperpolarizing factor</topic><topic>Forearm - blood supply</topic><topic>Humans</topic><topic>Infusions, Intravenous</topic><topic>Insulin resistance</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitroprusside - pharmacology</topic><topic>Obesity</topic><topic>Obesity - physiopathology</topic><topic>Ouabain - pharmacology</topic><topic>Plethysmography</topic><topic>Potassium - pharmacology</topic><topic>Potassium channels</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vigili de Kreutzenberg, S.</creatorcontrib><creatorcontrib>Kiwanuka, E.</creatorcontrib><creatorcontrib>Tiengo, A.</creatorcontrib><creatorcontrib>Avogaro, A.</creatorcontrib><collection>Istex</collection><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>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vigili de Kreutzenberg, S.</au><au>Kiwanuka, E.</au><au>Tiengo, A.</au><au>Avogaro, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Visceral obesity is characterized by impaired nitric oxide-independent vasodilation</atitle><jtitle>European heart journal</jtitle><addtitle>Eur Heart J</addtitle><date>2003-07-01</date><risdate>2003</risdate><volume>24</volume><issue>13</issue><spage>1210</spage><epage>1215</epage><pages>1210-1215</pages><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract>Background Endothelial dysfunction has been described in obesity. This study examines the impact of visceral obesity on nitric oxide-independent relaxation in the human forearm. Methods and results In ten viscerally obese and ten matched controls forearm blood flow (FBF) was measured by venous occlusion plethysmography during intrabrachial infusion of: (1) sodium nitroprusside; (2) bradykinin, before and after inhibition of vasoactive prostaglandins and nitric oxide; (3) potassium; (4) ouabain (Na+/K+ATPase inhibitor) alone or (5) in combination with BaCl2(KIRinhibitor). Baseline FBF and endothelium-independent vasodilatation were similar in the two groups. In obese patients, bradykinin-induced increase of FBF was significantly less than in controls (P<0.01). Irrespective of prostaglandins and nitric oxide inhibition, bradykinin response was lower in the viscerally obese. Intrabrachial potassium determined a significantly blunted response (P<0.05). Ouabain caused a similar, moderate decrease in basal FBF in the two groups; the coinfusion of BaCl2caused a more intense decline in FBF which was significantly relevant in obese (−24±5%, P<0.01). Conclusions In obese patients there is a blunted nitric oxide-independent relaxation determined by a decreased response of inwardly rectifying potassium channels.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>12831815</pmid><doi>10.1016/S0195-668X(03)00206-9</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Barium Compounds - pharmacology Biological and medical sciences Brachial Artery Bradykinin - pharmacology Cardiology. Vascular system Chlorides - pharmacology Cyclooxygenase Inhibitors - pharmacology Dose-Response Relationship, Drug Endothelium Endothelium, Vascular Endothelium-derived hyperpolarizing factor Forearm - blood supply Humans Infusions, Intravenous Insulin resistance Male Medical sciences Nitric Oxide - physiology Nitric Oxide Synthase - antagonists & inhibitors Nitroprusside - pharmacology Obesity Obesity - physiopathology Ouabain - pharmacology Plethysmography Potassium - pharmacology Potassium channels Vasodilation - drug effects Vasodilation - physiology Vasodilator Agents - pharmacology |
title | Visceral obesity is characterized by impaired nitric oxide-independent vasodilation |
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