Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase
Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha, Nebraska 68198-4575 The first goal of this study was to determine whether chronic injection of nicotine alters endothelium-dependent arteriolar dilatation. We measured the diameter of cheek pouch resistance arteri...
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Veröffentlicht in: | Journal of applied physiology (1985) 1999-04, Vol.86 (4), p.1126-1134 |
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creator | Mayhan, William G Sharpe, Glenda M |
description | Department of Physiology and Biophysics, University of Nebraska
Medical Center, Omaha, Nebraska 68198-4575
The first goal of this study was to determine
whether chronic injection of nicotine alters endothelium-dependent
arteriolar dilatation. We measured the diameter of cheek pouch
resistance arterioles (~50 µm in diameter) in response to
endothelium-dependent (acetylcholine and ADP) and -independent
(nitroglycerin) agonists in control hamsters and hamsters treated with
nicotine (2 µg · kg 1 · day 1
for 2-3 wk). In control hamsters, acetylcholine (0.1 and 1.0 µM) dilated arterioles by 13 ± 2 and 31 ± 3%,
respectively, and ADP (1.0 and 10 µM) dilated arterioles by 18 ± 1 and 30 ± 1%, respectively. In contrast,
acetylcholine (0.1 and 1.0 µM) dilated arterioles by only 5 ± 2 and 12 ± 3%, respectively, and ADP (1.0 and 10 µM) dilated
arterioles by only 7 ± 2 and 13 ± 3%, respectively, in animals
treated with nicotine ( P |
doi_str_mv | 10.1152/jappl.1999.86.4.1126 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pasca</sourceid><recordid>TN_cdi_proquest_journals_222199017</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>69675391</sourcerecordid><originalsourceid>FETCH-LOGICAL-c503t-2d441cf69eb68136f0bdba7f86750e5dda25073a438d2f023b4fe48010a598a03</originalsourceid><addsrcrecordid>eNp1kcuKFDEUhoMoTjv6BiJBRNxUm1vd3Enj6MDAbGbWIVU5mUqTqpRJCrvf3pTdeINZhZPz_ef2I_Saki2lJfu4V_PstrRt221TbUX-ZNUTtMkpVtCK0Kdo09QlKeqyqS_Qixj3hFAhSvocXVBCW0FbvkF-NwQ_2R7DYfZxCYCTxzn2yU6AlUsQIoZJ-zSAs8tYaJhzCFPCKuSk9U4FrK1TSSXrp08YjIE-YW9wXGYI_mA1ZCCOS1IRXqJnRrkIr87vJbq_-nK3-1bc3H693n2-KfqS8FQwLQTtTdVCVzWUV4Z0ulO1aaq8EpRaK1aSmivBG80MYbwTBkRDKFFl2yjCL9H7U905-O8LxCRHG3twTk3glyirNlfiLc3g2__AvV_ClGeTjLF8XkLrDIkT1AcfYwAj52BHFY6SErm6IX-5IVc3ZFNJIVc3suzNufbSjaD_Ep3On4F3Z0DFXjkT1NTb-Iera87oOuOHEzbYh-GHDSDn4Rjz6f3Dce38T0vxOHq1OHcHh7RqfkvkrA3_Ce01tuU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>222199017</pqid></control><display><type>article</type><title>Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase</title><source>MEDLINE</source><source>American Physiological Society</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Mayhan, William G ; Sharpe, Glenda M</creator><creatorcontrib>Mayhan, William G ; Sharpe, Glenda M</creatorcontrib><description>Department of Physiology and Biophysics, University of Nebraska
Medical Center, Omaha, Nebraska 68198-4575
The first goal of this study was to determine
whether chronic injection of nicotine alters endothelium-dependent
arteriolar dilatation. We measured the diameter of cheek pouch
resistance arterioles (~50 µm in diameter) in response to
endothelium-dependent (acetylcholine and ADP) and -independent
(nitroglycerin) agonists in control hamsters and hamsters treated with
nicotine (2 µg · kg 1 · day 1
for 2-3 wk). In control hamsters, acetylcholine (0.1 and 1.0 µM) dilated arterioles by 13 ± 2 and 31 ± 3%,
respectively, and ADP (1.0 and 10 µM) dilated arterioles by 18 ± 1 and 30 ± 1%, respectively. In contrast,
acetylcholine (0.1 and 1.0 µM) dilated arterioles by only 5 ± 2 and 12 ± 3%, respectively, and ADP (1.0 and 10 µM) dilated
arterioles by only 7 ± 2 and 13 ± 3%, respectively, in animals
treated with nicotine ( P < 0.05 vs.
response in control hamsters). Nitroglycerin produced similar
dose-related dilatation of cheek pouch arterioles in control and
nicotine-treated hamsters. Our second goal was to examine a possible
mechanism for impaired endothelium-dependent arteriolar dilatation
during chronic treatment with nicotine. We found that superfusion of
the cheek pouch microcirculation with superoxide dismutase (150 U/ml)
restored impaired endothelium-dependent, but did not alter
endothelium-independent, arteriolar dilatation in hamsters treated with
nicotine. Superfusion with superoxide dismutase did not alter
endothelium-dependent or -independent arteriolar dilatation in control
hamsters. We suggest that chronic exposure to nicotine produces
selective impairment of endothelium-dependent arteriolar dilatation via
a mechanism related to the synthesis/release of oxygen-derived free radicals.
acetylcholine; adenosine 5'-diphosphate; nitroglycerin; cheek
pouch; hamsters; arterioles; endothelium-derived relaxing factor; oxygen radicals; N G -monomethyl- L -arginine; nitric oxide</description><identifier>ISSN: 8750-7587</identifier><identifier>EISSN: 1522-1601</identifier><identifier>DOI: 10.1152/jappl.1999.86.4.1126</identifier><identifier>PMID: 10194193</identifier><identifier>CODEN: JAPHEV</identifier><language>eng</language><publisher>Bethesda, MD: Am Physiological Soc</publisher><subject>Acetylcholine - pharmacology ; Adenosine Diphosphate - pharmacology ; Animals ; Arterioles - drug effects ; Arterioles - physiology ; Biological and medical sciences ; Cheek ; Coronary vessels ; Cricetinae ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Male ; Medical research ; Medical sciences ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - physiology ; Nicotine ; Nicotine - pharmacology ; Nitroglycerin - pharmacology ; omega-N-Methylarginine - pharmacology ; Rodents ; Superoxide Dismutase - metabolism ; Superoxide Dismutase - pharmacology ; Tobacco, tobacco smoking ; Toxicology ; Vasodilation - drug effects ; Vasodilation - physiology</subject><ispartof>Journal of applied physiology (1985), 1999-04, Vol.86 (4), p.1126-1134</ispartof><rights>1999 INIST-CNRS</rights><rights>Copyright American Physiological Society Apr 1999</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-2d441cf69eb68136f0bdba7f86750e5dda25073a438d2f023b4fe48010a598a03</citedby><cites>FETCH-LOGICAL-c503t-2d441cf69eb68136f0bdba7f86750e5dda25073a438d2f023b4fe48010a598a03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1773211$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10194193$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mayhan, William G</creatorcontrib><creatorcontrib>Sharpe, Glenda M</creatorcontrib><title>Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>Department of Physiology and Biophysics, University of Nebraska
Medical Center, Omaha, Nebraska 68198-4575
The first goal of this study was to determine
whether chronic injection of nicotine alters endothelium-dependent
arteriolar dilatation. We measured the diameter of cheek pouch
resistance arterioles (~50 µm in diameter) in response to
endothelium-dependent (acetylcholine and ADP) and -independent
(nitroglycerin) agonists in control hamsters and hamsters treated with
nicotine (2 µg · kg 1 · day 1
for 2-3 wk). In control hamsters, acetylcholine (0.1 and 1.0 µM) dilated arterioles by 13 ± 2 and 31 ± 3%,
respectively, and ADP (1.0 and 10 µM) dilated arterioles by 18 ± 1 and 30 ± 1%, respectively. In contrast,
acetylcholine (0.1 and 1.0 µM) dilated arterioles by only 5 ± 2 and 12 ± 3%, respectively, and ADP (1.0 and 10 µM) dilated
arterioles by only 7 ± 2 and 13 ± 3%, respectively, in animals
treated with nicotine ( P < 0.05 vs.
response in control hamsters). Nitroglycerin produced similar
dose-related dilatation of cheek pouch arterioles in control and
nicotine-treated hamsters. Our second goal was to examine a possible
mechanism for impaired endothelium-dependent arteriolar dilatation
during chronic treatment with nicotine. We found that superfusion of
the cheek pouch microcirculation with superoxide dismutase (150 U/ml)
restored impaired endothelium-dependent, but did not alter
endothelium-independent, arteriolar dilatation in hamsters treated with
nicotine. Superfusion with superoxide dismutase did not alter
endothelium-dependent or -independent arteriolar dilatation in control
hamsters. We suggest that chronic exposure to nicotine produces
selective impairment of endothelium-dependent arteriolar dilatation via
a mechanism related to the synthesis/release of oxygen-derived free radicals.
acetylcholine; adenosine 5'-diphosphate; nitroglycerin; cheek
pouch; hamsters; arterioles; endothelium-derived relaxing factor; oxygen radicals; N G -monomethyl- L -arginine; nitric oxide</description><subject>Acetylcholine - pharmacology</subject><subject>Adenosine Diphosphate - pharmacology</subject><subject>Animals</subject><subject>Arterioles - drug effects</subject><subject>Arterioles - physiology</subject><subject>Biological and medical sciences</subject><subject>Cheek</subject><subject>Coronary vessels</subject><subject>Cricetinae</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiology</subject><subject>Male</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>Nicotine</subject><subject>Nicotine - pharmacology</subject><subject>Nitroglycerin - pharmacology</subject><subject>omega-N-Methylarginine - pharmacology</subject><subject>Rodents</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxide Dismutase - pharmacology</subject><subject>Tobacco, tobacco smoking</subject><subject>Toxicology</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><issn>8750-7587</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kcuKFDEUhoMoTjv6BiJBRNxUm1vd3Enj6MDAbGbWIVU5mUqTqpRJCrvf3pTdeINZhZPz_ef2I_Saki2lJfu4V_PstrRt221TbUX-ZNUTtMkpVtCK0Kdo09QlKeqyqS_Qixj3hFAhSvocXVBCW0FbvkF-NwQ_2R7DYfZxCYCTxzn2yU6AlUsQIoZJ-zSAs8tYaJhzCFPCKuSk9U4FrK1TSSXrp08YjIE-YW9wXGYI_mA1ZCCOS1IRXqJnRrkIr87vJbq_-nK3-1bc3H693n2-KfqS8FQwLQTtTdVCVzWUV4Z0ulO1aaq8EpRaK1aSmivBG80MYbwTBkRDKFFl2yjCL9H7U905-O8LxCRHG3twTk3glyirNlfiLc3g2__AvV_ClGeTjLF8XkLrDIkT1AcfYwAj52BHFY6SErm6IX-5IVc3ZFNJIVc3suzNufbSjaD_Ep3On4F3Z0DFXjkT1NTb-Iera87oOuOHEzbYh-GHDSDn4Rjz6f3Dce38T0vxOHq1OHcHh7RqfkvkrA3_Ce01tuU</recordid><startdate>19990401</startdate><enddate>19990401</enddate><creator>Mayhan, William G</creator><creator>Sharpe, Glenda M</creator><general>Am Physiological Soc</general><general>American Physiological Society</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19990401</creationdate><title>Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase</title><author>Mayhan, William G ; Sharpe, Glenda M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-2d441cf69eb68136f0bdba7f86750e5dda25073a438d2f023b4fe48010a598a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Adenosine Diphosphate - pharmacology</topic><topic>Animals</topic><topic>Arterioles - drug effects</topic><topic>Arterioles - physiology</topic><topic>Biological and medical sciences</topic><topic>Cheek</topic><topic>Coronary vessels</topic><topic>Cricetinae</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiology</topic><topic>Male</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Nicotine</topic><topic>Nicotine - pharmacology</topic><topic>Nitroglycerin - pharmacology</topic><topic>omega-N-Methylarginine - pharmacology</topic><topic>Rodents</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Superoxide Dismutase - pharmacology</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mayhan, William G</creatorcontrib><creatorcontrib>Sharpe, Glenda M</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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mayhan, William G</au><au>Sharpe, Glenda M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>1999-04-01</date><risdate>1999</risdate><volume>86</volume><issue>4</issue><spage>1126</spage><epage>1134</epage><pages>1126-1134</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><coden>JAPHEV</coden><abstract>Department of Physiology and Biophysics, University of Nebraska
Medical Center, Omaha, Nebraska 68198-4575
The first goal of this study was to determine
whether chronic injection of nicotine alters endothelium-dependent
arteriolar dilatation. We measured the diameter of cheek pouch
resistance arterioles (~50 µm in diameter) in response to
endothelium-dependent (acetylcholine and ADP) and -independent
(nitroglycerin) agonists in control hamsters and hamsters treated with
nicotine (2 µg · kg 1 · day 1
for 2-3 wk). In control hamsters, acetylcholine (0.1 and 1.0 µM) dilated arterioles by 13 ± 2 and 31 ± 3%,
respectively, and ADP (1.0 and 10 µM) dilated arterioles by 18 ± 1 and 30 ± 1%, respectively. In contrast,
acetylcholine (0.1 and 1.0 µM) dilated arterioles by only 5 ± 2 and 12 ± 3%, respectively, and ADP (1.0 and 10 µM) dilated
arterioles by only 7 ± 2 and 13 ± 3%, respectively, in animals
treated with nicotine ( P < 0.05 vs.
response in control hamsters). Nitroglycerin produced similar
dose-related dilatation of cheek pouch arterioles in control and
nicotine-treated hamsters. Our second goal was to examine a possible
mechanism for impaired endothelium-dependent arteriolar dilatation
during chronic treatment with nicotine. We found that superfusion of
the cheek pouch microcirculation with superoxide dismutase (150 U/ml)
restored impaired endothelium-dependent, but did not alter
endothelium-independent, arteriolar dilatation in hamsters treated with
nicotine. Superfusion with superoxide dismutase did not alter
endothelium-dependent or -independent arteriolar dilatation in control
hamsters. We suggest that chronic exposure to nicotine produces
selective impairment of endothelium-dependent arteriolar dilatation via
a mechanism related to the synthesis/release of oxygen-derived free radicals.
acetylcholine; adenosine 5'-diphosphate; nitroglycerin; cheek
pouch; hamsters; arterioles; endothelium-derived relaxing factor; oxygen radicals; N G -monomethyl- L -arginine; nitric oxide</abstract><cop>Bethesda, MD</cop><pub>Am Physiological Soc</pub><pmid>10194193</pmid><doi>10.1152/jappl.1999.86.4.1126</doi><tpages>9</tpages></addata></record> |
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language | eng |
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source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
subjects | Acetylcholine - pharmacology Adenosine Diphosphate - pharmacology Animals Arterioles - drug effects Arterioles - physiology Biological and medical sciences Cheek Coronary vessels Cricetinae Endothelium, Vascular - drug effects Endothelium, Vascular - physiology Male Medical research Medical sciences Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - physiology Nicotine Nicotine - pharmacology Nitroglycerin - pharmacology omega-N-Methylarginine - pharmacology Rodents Superoxide Dismutase - metabolism Superoxide Dismutase - pharmacology Tobacco, tobacco smoking Toxicology Vasodilation - drug effects Vasodilation - physiology |
title | Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase |
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