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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
Main Authors: Vigili de Kreutzenberg, S., Kiwanuka, E., Tiengo, A., Avogaro, A.
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Kiwanuka, E.
Tiengo, A.
Avogaro, A.
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
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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&lt;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&lt;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&lt;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 &amp; 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&amp;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&lt;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&lt;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&lt;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 &amp; 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 &amp; 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&lt;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&lt;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&lt;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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source Oxford Journals Online
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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