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Role for Hydrogen Peroxide in Flow-Induced Dilation of Human Coronary Arterioles
ABSTRACT—Flow-induced dilation (FID) is dependent largely on hyperpolarization of vascular smooth muscle cells (VSMCs) in human coronary arterioles (HCA) from patients with coronary disease. Animal studies show that shear stress induces endothelial generation of hydrogen peroxide (H2O2), which is pr...
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| Published in: | Circulation research 2003-02, Vol.92 (2), p.e31-e40 |
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| creator | Miura, Hiroto Bosnjak, John J Ning, Gang Saito, Takashi Miura, Mamoru Gutterman, David D |
| description | ABSTRACT—Flow-induced dilation (FID) is dependent largely on hyperpolarization of vascular smooth muscle cells (VSMCs) in human coronary arterioles (HCA) from patients with coronary disease. Animal studies show that shear stress induces endothelial generation of hydrogen peroxide (H2O2), which is proposed as an endothelium-derived hyperpolarizing factor (EDHF). We tested the hypothesis that H2O2 contributes to FID in HCA. Arterioles (135±7 μm, n=71) were dissected from human right atrial appendages at the time of cardiac surgery and cannulated with glass micropipettes. Changes in internal diameter and membrane potential of VSMCs to shear stress, H2O2, or to papaverine were recorded with videomicroscopy. In some vessels, endothelial H2O2 generation to shear stress was monitored directly using confocal microscopy with 2′,7′-dichlorofluorescin diacetate (DCFH) or using electron microscopy with cerium chloride. Catalase inhibited FID (%max dilation; 66±8 versus 25±7%;P |
| doi_str_mv | 10.1161/01.RES.0000054200.44505.AB |
| format | article |
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Animal studies show that shear stress induces endothelial generation of hydrogen peroxide (H2O2), which is proposed as an endothelium-derived hyperpolarizing factor (EDHF). We tested the hypothesis that H2O2 contributes to FID in HCA. Arterioles (135±7 μm, n=71) were dissected from human right atrial appendages at the time of cardiac surgery and cannulated with glass micropipettes. Changes in internal diameter and membrane potential of VSMCs to shear stress, H2O2, or to papaverine were recorded with videomicroscopy. In some vessels, endothelial H2O2 generation to shear stress was monitored directly using confocal microscopy with 2′,7′-dichlorofluorescin diacetate (DCFH) or using electron microscopy with cerium chloride. Catalase inhibited FID (%max dilation; 66±8 versus 25±7%;P <0.05, n=6), whereas dilation to papaverine was unchanged. Shear stress immediately increased DCFH fluorescence in the endothelial cell layer, whereas treatment with catalase abolished the increase in fluorescence. Electron microscopy with cerium chloride revealed shear stress–induced increase in cerium deposition in intimal area surrounding endothelial cells. Exogenous H2O2 dilated (%max dilation; 97±1%, ED50; 3.0±0.7×10 mol/L) and hyperpolarized HCA. Dilation to H2O2 was reduced by catalase, 40 mmol/L KCl, or charybdotoxin plus apamin, whereas endothelial denudation, deferoxamine, 1H--oxadiazole-[4,3-a]quinoxalin-1-one, or glibenclamide had no effect. These data provide evidence that shear stress induces endothelial release of H2O2 and are consistent with the idea that H2O2 is an EDHF that contributes to FID in HCA from patients with heart disease. The full text of this article is available at http://www.circresaha.org.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.0000054200.44505.AB</identifier><identifier>PMID: 12574154</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Apamin - pharmacology ; Arterioles - drug effects ; Arterioles - physiology ; Arterioles - ultrastructure ; Catalase - pharmacology ; Cerium ; Coronary Vessels - drug effects ; Coronary Vessels - physiology ; Enzyme Inhibitors - pharmacology ; Fluorescent Dyes ; Glyburide - pharmacology ; Humans ; Hydrogen Peroxide - metabolism ; Hydrogen Peroxide - pharmacology ; In Vitro Techniques ; Iron Chelating Agents - pharmacology ; Membrane Potentials - drug effects ; Membrane Potentials - physiology ; Microscopy, Confocal ; Microscopy, Electron ; Microscopy, Video ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - ultrastructure ; Oxidants - metabolism ; Oxidants - pharmacology ; Papaverine - pharmacology ; Potassium Channel Blockers - pharmacology ; Stress, Mechanical ; Vasodilation - drug effects ; Vasodilation - physiology ; Vasodilator Agents - pharmacology</subject><ispartof>Circulation research, 2003-02, Vol.92 (2), p.e31-e40</ispartof><rights>2003 American Heart Association, Inc.</rights><rights>Copyright American Heart Association, Inc. Feb 7 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5981-54cf9b964285963ee941fa8a93b559a7da40ffa63047aeb8abd94f90ebac45173</citedby><cites>FETCH-LOGICAL-c5981-54cf9b964285963ee941fa8a93b559a7da40ffa63047aeb8abd94f90ebac45173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12574154$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miura, Hiroto</creatorcontrib><creatorcontrib>Bosnjak, John J</creatorcontrib><creatorcontrib>Ning, Gang</creatorcontrib><creatorcontrib>Saito, Takashi</creatorcontrib><creatorcontrib>Miura, Mamoru</creatorcontrib><creatorcontrib>Gutterman, David D</creatorcontrib><title>Role for Hydrogen Peroxide in Flow-Induced Dilation of Human Coronary Arterioles</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>ABSTRACT—Flow-induced dilation (FID) is dependent largely on hyperpolarization of vascular smooth muscle cells (VSMCs) in human coronary arterioles (HCA) from patients with coronary disease. Animal studies show that shear stress induces endothelial generation of hydrogen peroxide (H2O2), which is proposed as an endothelium-derived hyperpolarizing factor (EDHF). We tested the hypothesis that H2O2 contributes to FID in HCA. Arterioles (135±7 μm, n=71) were dissected from human right atrial appendages at the time of cardiac surgery and cannulated with glass micropipettes. Changes in internal diameter and membrane potential of VSMCs to shear stress, H2O2, or to papaverine were recorded with videomicroscopy. In some vessels, endothelial H2O2 generation to shear stress was monitored directly using confocal microscopy with 2′,7′-dichlorofluorescin diacetate (DCFH) or using electron microscopy with cerium chloride. Catalase inhibited FID (%max dilation; 66±8 versus 25±7%;P <0.05, n=6), whereas dilation to papaverine was unchanged. Shear stress immediately increased DCFH fluorescence in the endothelial cell layer, whereas treatment with catalase abolished the increase in fluorescence. Electron microscopy with cerium chloride revealed shear stress–induced increase in cerium deposition in intimal area surrounding endothelial cells. Exogenous H2O2 dilated (%max dilation; 97±1%, ED50; 3.0±0.7×10 mol/L) and hyperpolarized HCA. Dilation to H2O2 was reduced by catalase, 40 mmol/L KCl, or charybdotoxin plus apamin, whereas endothelial denudation, deferoxamine, 1H--oxadiazole-[4,3-a]quinoxalin-1-one, or glibenclamide had no effect. These data provide evidence that shear stress induces endothelial release of H2O2 and are consistent with the idea that H2O2 is an EDHF that contributes to FID in HCA from patients with heart disease. The full text of this article is available at http://www.circresaha.org.</description><subject>Apamin - pharmacology</subject><subject>Arterioles - drug effects</subject><subject>Arterioles - physiology</subject><subject>Arterioles - ultrastructure</subject><subject>Catalase - pharmacology</subject><subject>Cerium</subject><subject>Coronary Vessels - drug effects</subject><subject>Coronary Vessels - physiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fluorescent Dyes</subject><subject>Glyburide - pharmacology</subject><subject>Humans</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Iron Chelating Agents - pharmacology</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Potentials - physiology</subject><subject>Microscopy, Confocal</subject><subject>Microscopy, Electron</subject><subject>Microscopy, Video</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Muscle, Smooth, Vascular - ultrastructure</subject><subject>Oxidants - metabolism</subject><subject>Oxidants - pharmacology</subject><subject>Papaverine - pharmacology</subject><subject>Potassium Channel Blockers - pharmacology</subject><subject>Stress, Mechanical</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNpFkNtOwzAMhiMEgnF4BRRx32LnsDbcjbExJCSmAddR2iZQ6BpIV429PRmbhG8s2b9_2x8hVwgp4hCvAdPF5DmFbUjBAFIhJMh0dHtABiiZSITM8JAMYl8lGedwQk677gMABWfqmJwgk5lAKQZkvvCNpc4HOttUwb_Zls5t8D91ZWnd0mnj18lDW_Wlrehd3ZhV7VvqHZ31S9PSsQ--NWFDR2FlQx2tunNy5EzT2Yt9PiOv08nLeJY8Pt0_jEePSSlVjokUpVOFGgqWSzXk1iqBzuRG8UJKZbLKCHDODDmIzNgiN0WlhFNgC1MKiRk_I1c736_gv3vbrfSH70MbV2qGLP7Jcx5FNztRGXzXBev0V6iX8WCNoLcsNaCOLPU_S_3HUo9u4_DlfkNfLG31P7qHFwViJ1j7Jr7ffTb92gb9bk2zev-z5IAsYdvMIIMkVhjyXyzVfuM</recordid><startdate>20030207</startdate><enddate>20030207</enddate><creator>Miura, Hiroto</creator><creator>Bosnjak, John J</creator><creator>Ning, Gang</creator><creator>Saito, Takashi</creator><creator>Miura, Mamoru</creator><creator>Gutterman, David D</creator><general>American Heart Association, Inc</general><general>Lippincott Williams & Wilkins Ovid Technologies</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope></search><sort><creationdate>20030207</creationdate><title>Role for Hydrogen Peroxide in Flow-Induced Dilation of Human Coronary Arterioles</title><author>Miura, Hiroto ; Bosnjak, John J ; Ning, Gang ; Saito, Takashi ; Miura, Mamoru ; Gutterman, David D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5981-54cf9b964285963ee941fa8a93b559a7da40ffa63047aeb8abd94f90ebac45173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Apamin - pharmacology</topic><topic>Arterioles - drug effects</topic><topic>Arterioles - physiology</topic><topic>Arterioles - ultrastructure</topic><topic>Catalase - pharmacology</topic><topic>Cerium</topic><topic>Coronary Vessels - drug effects</topic><topic>Coronary Vessels - physiology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fluorescent Dyes</topic><topic>Glyburide - pharmacology</topic><topic>Humans</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Iron Chelating Agents - pharmacology</topic><topic>Membrane Potentials - drug effects</topic><topic>Membrane Potentials - physiology</topic><topic>Microscopy, Confocal</topic><topic>Microscopy, Electron</topic><topic>Microscopy, Video</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Muscle, Smooth, Vascular - ultrastructure</topic><topic>Oxidants - metabolism</topic><topic>Oxidants - pharmacology</topic><topic>Papaverine - pharmacology</topic><topic>Potassium Channel Blockers - pharmacology</topic><topic>Stress, Mechanical</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miura, Hiroto</creatorcontrib><creatorcontrib>Bosnjak, John J</creatorcontrib><creatorcontrib>Ning, Gang</creatorcontrib><creatorcontrib>Saito, Takashi</creatorcontrib><creatorcontrib>Miura, Mamoru</creatorcontrib><creatorcontrib>Gutterman, David D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miura, Hiroto</au><au>Bosnjak, John J</au><au>Ning, Gang</au><au>Saito, Takashi</au><au>Miura, Mamoru</au><au>Gutterman, David D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role for Hydrogen Peroxide in Flow-Induced Dilation of Human Coronary Arterioles</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2003-02-07</date><risdate>2003</risdate><volume>92</volume><issue>2</issue><spage>e31</spage><epage>e40</epage><pages>e31-e40</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>ABSTRACT—Flow-induced dilation (FID) is dependent largely on hyperpolarization of vascular smooth muscle cells (VSMCs) in human coronary arterioles (HCA) from patients with coronary disease. Animal studies show that shear stress induces endothelial generation of hydrogen peroxide (H2O2), which is proposed as an endothelium-derived hyperpolarizing factor (EDHF). We tested the hypothesis that H2O2 contributes to FID in HCA. Arterioles (135±7 μm, n=71) were dissected from human right atrial appendages at the time of cardiac surgery and cannulated with glass micropipettes. Changes in internal diameter and membrane potential of VSMCs to shear stress, H2O2, or to papaverine were recorded with videomicroscopy. In some vessels, endothelial H2O2 generation to shear stress was monitored directly using confocal microscopy with 2′,7′-dichlorofluorescin diacetate (DCFH) or using electron microscopy with cerium chloride. Catalase inhibited FID (%max dilation; 66±8 versus 25±7%;P <0.05, n=6), whereas dilation to papaverine was unchanged. Shear stress immediately increased DCFH fluorescence in the endothelial cell layer, whereas treatment with catalase abolished the increase in fluorescence. Electron microscopy with cerium chloride revealed shear stress–induced increase in cerium deposition in intimal area surrounding endothelial cells. Exogenous H2O2 dilated (%max dilation; 97±1%, ED50; 3.0±0.7×10 mol/L) and hyperpolarized HCA. Dilation to H2O2 was reduced by catalase, 40 mmol/L KCl, or charybdotoxin plus apamin, whereas endothelial denudation, deferoxamine, 1H--oxadiazole-[4,3-a]quinoxalin-1-one, or glibenclamide had no effect. These data provide evidence that shear stress induces endothelial release of H2O2 and are consistent with the idea that H2O2 is an EDHF that contributes to FID in HCA from patients with heart disease. The full text of this article is available at http://www.circresaha.org.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>12574154</pmid><doi>10.1161/01.RES.0000054200.44505.AB</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Apamin - pharmacology Arterioles - drug effects Arterioles - physiology Arterioles - ultrastructure Catalase - pharmacology Cerium Coronary Vessels - drug effects Coronary Vessels - physiology Enzyme Inhibitors - pharmacology Fluorescent Dyes Glyburide - pharmacology Humans Hydrogen Peroxide - metabolism Hydrogen Peroxide - pharmacology In Vitro Techniques Iron Chelating Agents - pharmacology Membrane Potentials - drug effects Membrane Potentials - physiology Microscopy, Confocal Microscopy, Electron Microscopy, Video Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - ultrastructure Oxidants - metabolism Oxidants - pharmacology Papaverine - pharmacology Potassium Channel Blockers - pharmacology Stress, Mechanical Vasodilation - drug effects Vasodilation - physiology Vasodilator Agents - pharmacology |
| title | Role for Hydrogen Peroxide in Flow-Induced Dilation of Human Coronary Arterioles |
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