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Recovery by ascorbate of impaired nitric oxide‐dependent relaxation resulting from oxidant stress in rat aorta
1 In this study we investigated the ability of ascorbate to protect nitric oxide from destruction by superoxide anion. 2 Ascorbate produced concentration‐dependent relaxation of rings of rat aorta, comprising two components: the first, seen at 1–300 μM, reached a maximum of 45.3±2.8%, and was abolis...
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Published in: | British journal of pharmacology 1998-10, Vol.125 (4), p.782-786 |
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description | 1
In this study we investigated the ability of ascorbate to protect nitric oxide from destruction by superoxide anion.
2
Ascorbate produced concentration‐dependent relaxation of rings of rat aorta, comprising two components: the first, seen at 1–300 μM, reached a maximum of 45.3±2.8%, and was abolished by endothelial removal or treatment with L‐NAME (100 μM), demonstrating involvement of nitric oxide. The second occurred at concentrations of 1 mM and above and was associated with falls in the pH of the bathing fluid.
3
Pretreatment with ascorbate at concentrations up to 3 mM had no effect on the relaxation to acetylcholine (10 nM–10 μM) on endothelium‐containing rings or adenosine (0.1 μM–3 mM) on endothelium‐denuded rings.
4
An oxidant stress was applied to aortic rings, comprising inhibition of endogenous Cu/Zn superoxide dismutase by diethyldithiocarbamate (0.1 mM) followed by generation of superoxide anion by hypoxanthine (0.1 mM/xanthine oxidase (16 u ml−1). This reduced maximal acetylcholine‐induced relaxation from 96.7±1.3% to 42.4±3.5% (P |
doi_str_mv | 10.1038/sj.bjp.0702120 |
format | article |
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In this study we investigated the ability of ascorbate to protect nitric oxide from destruction by superoxide anion.
2
Ascorbate produced concentration‐dependent relaxation of rings of rat aorta, comprising two components: the first, seen at 1–300 μM, reached a maximum of 45.3±2.8%, and was abolished by endothelial removal or treatment with L‐NAME (100 μM), demonstrating involvement of nitric oxide. The second occurred at concentrations of 1 mM and above and was associated with falls in the pH of the bathing fluid.
3
Pretreatment with ascorbate at concentrations up to 3 mM had no effect on the relaxation to acetylcholine (10 nM–10 μM) on endothelium‐containing rings or adenosine (0.1 μM–3 mM) on endothelium‐denuded rings.
4
An oxidant stress was applied to aortic rings, comprising inhibition of endogenous Cu/Zn superoxide dismutase by diethyldithiocarbamate (0.1 mM) followed by generation of superoxide anion by hypoxanthine (0.1 mM/xanthine oxidase (16 u ml−1). This reduced maximal acetylcholine‐induced relaxation from 96.7±1.3% to 42.4±3.5% (P<0.001). Treatment with ascorbate (30 μM–3 mM) reversed this blockade in a concentration‐dependent manner.
5
Our findings show that ascorbate has the ability to protect nitric oxide from destruction by superoxide anion. This action is seen with ascorbate at levels normally present in plasma, suggesting that this antioxidant may exert a tonic protective effect on nitric oxide within the vasculature.
British Journal of Pharmacology (1998) 125, 782–786; doi:10.1038/sj.bjp.0702120</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0702120</identifier><identifier>PMID: 9831915</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Acetylcholine - pharmacology ; Animals ; antioxidant ; Aorta - drug effects ; ascorbate ; Ascorbic Acid - metabolism ; Ascorbic Acid - pharmacology ; Biological and medical sciences ; Cardiovascular system ; Dose-Response Relationship, Drug ; Drug Interactions ; endothelium ; Endothelium, Vascular - physiology ; Female ; Medical sciences ; Miscellaneous ; Muscle Relaxation - drug effects ; Muscle, Smooth - drug effects ; Nitric oxide ; Nitric Oxide - pharmacology ; oxidant stress ; Oxidative Stress - physiology ; Pharmacology. Drug treatments ; Rats ; Rats, Wistar ; superoxide anion ; superoxide dismutase ; Superoxide Dismutase - drug effects ; superoxide dismutase mimetic ; Superoxides - pharmacology</subject><ispartof>British journal of pharmacology, 1998-10, Vol.125 (4), p.782-786</ispartof><rights>1998 British Pharmacological Society</rights><rights>1999 INIST-CNRS</rights><rights>Copyright 1998, Nature Publishing Group 1998 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4585-fffb15940647b17f679bbcd32f6beba1c04b897efc6305c99c78c3b07c42da473</citedby><cites>FETCH-LOGICAL-c4585-fffb15940647b17f679bbcd32f6beba1c04b897efc6305c99c78c3b07c42da473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1571043/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1571043/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1606860$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9831915$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dudgeon, Sinead</creatorcontrib><creatorcontrib>Benson, David P</creatorcontrib><creatorcontrib>MacKenzie, Andrew</creatorcontrib><creatorcontrib>Paisley‐Zyszkiewicz, Karen</creatorcontrib><creatorcontrib>Martin, William</creatorcontrib><title>Recovery by ascorbate of impaired nitric oxide‐dependent relaxation resulting from oxidant stress in rat aorta</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>1
In this study we investigated the ability of ascorbate to protect nitric oxide from destruction by superoxide anion.
2
Ascorbate produced concentration‐dependent relaxation of rings of rat aorta, comprising two components: the first, seen at 1–300 μM, reached a maximum of 45.3±2.8%, and was abolished by endothelial removal or treatment with L‐NAME (100 μM), demonstrating involvement of nitric oxide. The second occurred at concentrations of 1 mM and above and was associated with falls in the pH of the bathing fluid.
3
Pretreatment with ascorbate at concentrations up to 3 mM had no effect on the relaxation to acetylcholine (10 nM–10 μM) on endothelium‐containing rings or adenosine (0.1 μM–3 mM) on endothelium‐denuded rings.
4
An oxidant stress was applied to aortic rings, comprising inhibition of endogenous Cu/Zn superoxide dismutase by diethyldithiocarbamate (0.1 mM) followed by generation of superoxide anion by hypoxanthine (0.1 mM/xanthine oxidase (16 u ml−1). This reduced maximal acetylcholine‐induced relaxation from 96.7±1.3% to 42.4±3.5% (P<0.001). Treatment with ascorbate (30 μM–3 mM) reversed this blockade in a concentration‐dependent manner.
5
Our findings show that ascorbate has the ability to protect nitric oxide from destruction by superoxide anion. This action is seen with ascorbate at levels normally present in plasma, suggesting that this antioxidant may exert a tonic protective effect on nitric oxide within the vasculature.
British Journal of Pharmacology (1998) 125, 782–786; doi:10.1038/sj.bjp.0702120</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>antioxidant</subject><subject>Aorta - drug effects</subject><subject>ascorbate</subject><subject>Ascorbic Acid - metabolism</subject><subject>Ascorbic Acid - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cardiovascular system</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Interactions</subject><subject>endothelium</subject><subject>Endothelium, Vascular - physiology</subject><subject>Female</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>Muscle Relaxation - drug effects</subject><subject>Muscle, Smooth - drug effects</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - pharmacology</subject><subject>oxidant stress</subject><subject>Oxidative Stress - physiology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>superoxide anion</subject><subject>superoxide dismutase</subject><subject>Superoxide Dismutase - drug effects</subject><subject>superoxide dismutase mimetic</subject><subject>Superoxides - pharmacology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNqFkLFuFDEQhi0UlByBlg7JRdo9xmd77W0iQQQEKRIIkdoae-3g0956ZW9CruMReEaeBCd3CqRKZUvfN_-MfkJeM1gy4PptWS_telqCghVbwTOyYEK1jeSaHZAFAKiGMa2PyItS1gAVKnlIDjvNWcfkgkzfvEs3Pm-p3VIsLmWLs6cp0LiZMGbf0zHOOTqabmPv__z63fvJj70fZ5r9gLc4xzTWb7ke5jhe0ZDT5t7FapS5gkJjFXCmmPKML8nzgEPxr_bvMbn8-OH72Xlz8eXT57N3F40TUssmhGCZ7AS0QlmmQqs6a13PV6G13iJzIKzulA-u5SBd1zmlHbegnFj1KBQ_Jqe73Onabnzv6sEZBzPluMG8NQmjeUzG-MNcpRvDpGIgeA1Y7gJcTqVkHx5mGZi76k1Zm1q92VdfB978v_FB33dd-cme155xCBlHF8u_1BZa3d7F8J32Mw5--8RS8_7ruRQg-V8K2aJm</recordid><startdate>199810</startdate><enddate>199810</enddate><creator>Dudgeon, Sinead</creator><creator>Benson, David P</creator><creator>MacKenzie, Andrew</creator><creator>Paisley‐Zyszkiewicz, Karen</creator><creator>Martin, William</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</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>5PM</scope></search><sort><creationdate>199810</creationdate><title>Recovery by ascorbate of impaired nitric oxide‐dependent relaxation resulting from oxidant stress in rat aorta</title><author>Dudgeon, Sinead ; Benson, David P ; MacKenzie, Andrew ; Paisley‐Zyszkiewicz, Karen ; Martin, William</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4585-fffb15940647b17f679bbcd32f6beba1c04b897efc6305c99c78c3b07c42da473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>antioxidant</topic><topic>Aorta - drug effects</topic><topic>ascorbate</topic><topic>Ascorbic Acid - metabolism</topic><topic>Ascorbic Acid - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cardiovascular system</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Interactions</topic><topic>endothelium</topic><topic>Endothelium, Vascular - physiology</topic><topic>Female</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>Muscle Relaxation - drug effects</topic><topic>Muscle, Smooth - drug effects</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - pharmacology</topic><topic>oxidant stress</topic><topic>Oxidative Stress - physiology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>superoxide anion</topic><topic>superoxide dismutase</topic><topic>Superoxide Dismutase - drug effects</topic><topic>superoxide dismutase mimetic</topic><topic>Superoxides - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dudgeon, Sinead</creatorcontrib><creatorcontrib>Benson, David P</creatorcontrib><creatorcontrib>MacKenzie, Andrew</creatorcontrib><creatorcontrib>Paisley‐Zyszkiewicz, Karen</creatorcontrib><creatorcontrib>Martin, William</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>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dudgeon, Sinead</au><au>Benson, David P</au><au>MacKenzie, Andrew</au><au>Paisley‐Zyszkiewicz, Karen</au><au>Martin, William</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Recovery by ascorbate of impaired nitric oxide‐dependent relaxation resulting from oxidant stress in rat aorta</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1998-10</date><risdate>1998</risdate><volume>125</volume><issue>4</issue><spage>782</spage><epage>786</epage><pages>782-786</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>1
In this study we investigated the ability of ascorbate to protect nitric oxide from destruction by superoxide anion.
2
Ascorbate produced concentration‐dependent relaxation of rings of rat aorta, comprising two components: the first, seen at 1–300 μM, reached a maximum of 45.3±2.8%, and was abolished by endothelial removal or treatment with L‐NAME (100 μM), demonstrating involvement of nitric oxide. The second occurred at concentrations of 1 mM and above and was associated with falls in the pH of the bathing fluid.
3
Pretreatment with ascorbate at concentrations up to 3 mM had no effect on the relaxation to acetylcholine (10 nM–10 μM) on endothelium‐containing rings or adenosine (0.1 μM–3 mM) on endothelium‐denuded rings.
4
An oxidant stress was applied to aortic rings, comprising inhibition of endogenous Cu/Zn superoxide dismutase by diethyldithiocarbamate (0.1 mM) followed by generation of superoxide anion by hypoxanthine (0.1 mM/xanthine oxidase (16 u ml−1). This reduced maximal acetylcholine‐induced relaxation from 96.7±1.3% to 42.4±3.5% (P<0.001). Treatment with ascorbate (30 μM–3 mM) reversed this blockade in a concentration‐dependent manner.
5
Our findings show that ascorbate has the ability to protect nitric oxide from destruction by superoxide anion. This action is seen with ascorbate at levels normally present in plasma, suggesting that this antioxidant may exert a tonic protective effect on nitric oxide within the vasculature.
British Journal of Pharmacology (1998) 125, 782–786; doi:10.1038/sj.bjp.0702120</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>9831915</pmid><doi>10.1038/sj.bjp.0702120</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acetylcholine - pharmacology Animals antioxidant Aorta - drug effects ascorbate Ascorbic Acid - metabolism Ascorbic Acid - pharmacology Biological and medical sciences Cardiovascular system Dose-Response Relationship, Drug Drug Interactions endothelium Endothelium, Vascular - physiology Female Medical sciences Miscellaneous Muscle Relaxation - drug effects Muscle, Smooth - drug effects Nitric oxide Nitric Oxide - pharmacology oxidant stress Oxidative Stress - physiology Pharmacology. Drug treatments Rats Rats, Wistar superoxide anion superoxide dismutase Superoxide Dismutase - drug effects superoxide dismutase mimetic Superoxides - pharmacology |
title | Recovery by ascorbate of impaired nitric oxide‐dependent relaxation resulting from oxidant stress in rat aorta |
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