Endothelium-dependent contraction induced by nicotine in isolated canine basilar artery -possible involvement of a thromboxane A2 (TXA2) like substance
The present experiments were undertaken to determine whether the response to nicotine in the isolated canine cerebral artery is endothelium-dependent. Changes in the tension of arterial strips were recorded isometrically. Removal of the endothelium was carried out by gentle rubbing, and confirmed by...
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Veröffentlicht in: | Life sciences (1973) 1988, Vol.42 (4), p.437-445 |
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description | The present experiments were undertaken to determine whether the response to nicotine in the isolated canine cerebral artery is endothelium-dependent. Changes in the tension of arterial strips were recorded isometrically. Removal of the endothelium was carried out by gentle rubbing, and confirmed by scanning electron microscopy. Rubbing procedure did not affect the contractile response of the strips to serotonin. Treatment of unrubbed strips with nicotine (10(-4)M) caused a transient contraction. This response was abolished by removal of endothelium and attenuated by hexamethonium (5 x 10(-6)M) and atropine (10(-6)M). The nicotine-induced contraction was attenuated also by aspirin (5 x 10(-5)M), a cyclooxygenase inhibitor, OKY-046 (5 x 10(-5)M), a thromboxane A2 (TXA2) synthetase inhibitor and ONO-3708 (5 x 10(-9)M), a TXA2 antagonist. These results indicate that the nicotine-induced contraction in canine cerebral artery is endothelium-dependent, and suggest that the endothelium-derived contracting factor (EDCF) in the nicotine-induced response is a TXA2-like substance. |
doi_str_mv | 10.1016/0024-3205(88)90082-3 |
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Changes in the tension of arterial strips were recorded isometrically. Removal of the endothelium was carried out by gentle rubbing, and confirmed by scanning electron microscopy. Rubbing procedure did not affect the contractile response of the strips to serotonin. Treatment of unrubbed strips with nicotine (10(-4)M) caused a transient contraction. This response was abolished by removal of endothelium and attenuated by hexamethonium (5 x 10(-6)M) and atropine (10(-6)M). The nicotine-induced contraction was attenuated also by aspirin (5 x 10(-5)M), a cyclooxygenase inhibitor, OKY-046 (5 x 10(-5)M), a thromboxane A2 (TXA2) synthetase inhibitor and ONO-3708 (5 x 10(-9)M), a TXA2 antagonist. These results indicate that the nicotine-induced contraction in canine cerebral artery is endothelium-dependent, and suggest that the endothelium-derived contracting factor (EDCF) in the nicotine-induced response is a TXA2-like substance.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/0024-3205(88)90082-3</identifier><identifier>PMID: 2893233</identifier><identifier>CODEN: LIFSAK</identifier><language>eng</language><publisher>Amsterdam: Elsevier</publisher><subject>Animals ; Aspirin - pharmacology ; Atropine - pharmacology ; Basilar Artery - physiology ; Biological and medical sciences ; Dogs ; Endothelium, Vascular - physiology ; Female ; Hexamethonium ; Hexamethonium Compounds - pharmacology ; Male ; Medical sciences ; Methacrylates - pharmacology ; Microscopy, Electron, Scanning ; Muscle Contraction - drug effects ; Muscle, Smooth, Vascular - physiology ; Nicotine - pharmacology ; Phentolamine - pharmacology ; Physostigmine - pharmacology ; Serotonin - pharmacology ; Thromboxane A2 - analogs & derivatives ; Thromboxane A2 - antagonists & inhibitors ; Thromboxane A2 - pharmacology ; Thromboxane A2 - physiology ; Thromboxane-A Synthase - antagonists & inhibitors ; Tobacco, tobacco smoking ; Toxicology</subject><ispartof>Life sciences (1973), 1988, Vol.42 (4), p.437-445</ispartof><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-67b54fb70e17ed27298a1aed6acd95363a01ed2996d4805b7ca7462cb827f9873</citedby><cites>FETCH-LOGICAL-c397t-67b54fb70e17ed27298a1aed6acd95363a01ed2996d4805b7ca7462cb827f9873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7824644$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2893233$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SHIRAHASE, H</creatorcontrib><creatorcontrib>USUI, H</creatorcontrib><creatorcontrib>KURAHASHI, K</creatorcontrib><creatorcontrib>FUJIWARA, M</creatorcontrib><creatorcontrib>FUKUI, K</creatorcontrib><title>Endothelium-dependent contraction induced by nicotine in isolated canine basilar artery -possible involvement of a thromboxane A2 (TXA2) like substance</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>The present experiments were undertaken to determine whether the response to nicotine in the isolated canine cerebral artery is endothelium-dependent. Changes in the tension of arterial strips were recorded isometrically. Removal of the endothelium was carried out by gentle rubbing, and confirmed by scanning electron microscopy. Rubbing procedure did not affect the contractile response of the strips to serotonin. Treatment of unrubbed strips with nicotine (10(-4)M) caused a transient contraction. This response was abolished by removal of endothelium and attenuated by hexamethonium (5 x 10(-6)M) and atropine (10(-6)M). The nicotine-induced contraction was attenuated also by aspirin (5 x 10(-5)M), a cyclooxygenase inhibitor, OKY-046 (5 x 10(-5)M), a thromboxane A2 (TXA2) synthetase inhibitor and ONO-3708 (5 x 10(-9)M), a TXA2 antagonist. These results indicate that the nicotine-induced contraction in canine cerebral artery is endothelium-dependent, and suggest that the endothelium-derived contracting factor (EDCF) in the nicotine-induced response is a TXA2-like substance.</description><subject>Animals</subject><subject>Aspirin - pharmacology</subject><subject>Atropine - pharmacology</subject><subject>Basilar Artery - physiology</subject><subject>Biological and medical sciences</subject><subject>Dogs</subject><subject>Endothelium, Vascular - physiology</subject><subject>Female</subject><subject>Hexamethonium</subject><subject>Hexamethonium Compounds - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methacrylates - pharmacology</subject><subject>Microscopy, Electron, Scanning</subject><subject>Muscle Contraction - drug effects</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>Nicotine - pharmacology</subject><subject>Phentolamine - pharmacology</subject><subject>Physostigmine - pharmacology</subject><subject>Serotonin - pharmacology</subject><subject>Thromboxane A2 - analogs & derivatives</subject><subject>Thromboxane A2 - antagonists & inhibitors</subject><subject>Thromboxane A2 - pharmacology</subject><subject>Thromboxane A2 - physiology</subject><subject>Thromboxane-A Synthase - antagonists & inhibitors</subject><subject>Tobacco, tobacco smoking</subject><subject>Toxicology</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kctqHDEUREWIccZO_iABLUKwF53o0d2SloPxCwzZOJCd0KuxErU0kdTG8yX53ajjYVaCuqcK3VsAfMToK0Z4_IYQ6TtK0HDB-aVAiJOOvgEbzJno0EjxW7A5Iu_AWSm_EELDwOgpOCVcUELpBvy9jjbVJxf8MnfW7Vy0LlZoUqxZmepThD7axTgL9R5Gb1L10TUN-pKCqk03Kq6SVsUHlaHK1eU97HapFK_Dyj6n8OzmNTdNUMH6lNOs04tqri2BF48_t-QSBv_bwbLoUlU07j04mVQo7sPhPQc_bq4fr-66h--391fbh85QwWo3Mj30k2bIYeYsYURwhZWzozJWDHSkCuGmCzHanqNBM6NYPxKjOWGT4Iyegy-vubuc_iyuVDn7YlwI7XNpKZJxJHqKRAP7V9Dktlh2k9xlP6u8lxjJtQ-5Hluux5acy_99SNpsnw75i56dPZoOBbT558NcFaPClNvyvhwxxkk_9j39B_IilMk</recordid><startdate>1988</startdate><enddate>1988</enddate><creator>SHIRAHASE, H</creator><creator>USUI, H</creator><creator>KURAHASHI, K</creator><creator>FUJIWARA, M</creator><creator>FUKUI, K</creator><general>Elsevier</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>7X8</scope></search><sort><creationdate>1988</creationdate><title>Endothelium-dependent contraction induced by nicotine in isolated canine basilar artery -possible involvement of a thromboxane A2 (TXA2) like substance</title><author>SHIRAHASE, H ; USUI, H ; KURAHASHI, K ; FUJIWARA, M ; FUKUI, K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-67b54fb70e17ed27298a1aed6acd95363a01ed2996d4805b7ca7462cb827f9873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Animals</topic><topic>Aspirin - pharmacology</topic><topic>Atropine - pharmacology</topic><topic>Basilar Artery - physiology</topic><topic>Biological and medical sciences</topic><topic>Dogs</topic><topic>Endothelium, Vascular - physiology</topic><topic>Female</topic><topic>Hexamethonium</topic><topic>Hexamethonium Compounds - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methacrylates - pharmacology</topic><topic>Microscopy, Electron, Scanning</topic><topic>Muscle Contraction - drug effects</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Nicotine - pharmacology</topic><topic>Phentolamine - pharmacology</topic><topic>Physostigmine - pharmacology</topic><topic>Serotonin - pharmacology</topic><topic>Thromboxane A2 - analogs & derivatives</topic><topic>Thromboxane A2 - antagonists & inhibitors</topic><topic>Thromboxane A2 - pharmacology</topic><topic>Thromboxane A2 - physiology</topic><topic>Thromboxane-A Synthase - antagonists & inhibitors</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SHIRAHASE, H</creatorcontrib><creatorcontrib>USUI, H</creatorcontrib><creatorcontrib>KURAHASHI, K</creatorcontrib><creatorcontrib>FUJIWARA, M</creatorcontrib><creatorcontrib>FUKUI, K</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>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SHIRAHASE, H</au><au>USUI, H</au><au>KURAHASHI, K</au><au>FUJIWARA, M</au><au>FUKUI, K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelium-dependent contraction induced by nicotine in isolated canine basilar artery -possible involvement of a thromboxane A2 (TXA2) like substance</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>1988</date><risdate>1988</risdate><volume>42</volume><issue>4</issue><spage>437</spage><epage>445</epage><pages>437-445</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><coden>LIFSAK</coden><abstract>The present experiments were undertaken to determine whether the response to nicotine in the isolated canine cerebral artery is endothelium-dependent. Changes in the tension of arterial strips were recorded isometrically. Removal of the endothelium was carried out by gentle rubbing, and confirmed by scanning electron microscopy. Rubbing procedure did not affect the contractile response of the strips to serotonin. Treatment of unrubbed strips with nicotine (10(-4)M) caused a transient contraction. This response was abolished by removal of endothelium and attenuated by hexamethonium (5 x 10(-6)M) and atropine (10(-6)M). The nicotine-induced contraction was attenuated also by aspirin (5 x 10(-5)M), a cyclooxygenase inhibitor, OKY-046 (5 x 10(-5)M), a thromboxane A2 (TXA2) synthetase inhibitor and ONO-3708 (5 x 10(-9)M), a TXA2 antagonist. These results indicate that the nicotine-induced contraction in canine cerebral artery is endothelium-dependent, and suggest that the endothelium-derived contracting factor (EDCF) in the nicotine-induced response is a TXA2-like substance.</abstract><cop>Amsterdam</cop><pub>Elsevier</pub><pmid>2893233</pmid><doi>10.1016/0024-3205(88)90082-3</doi><tpages>9</tpages></addata></record> |
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subjects | Animals Aspirin - pharmacology Atropine - pharmacology Basilar Artery - physiology Biological and medical sciences Dogs Endothelium, Vascular - physiology Female Hexamethonium Hexamethonium Compounds - pharmacology Male Medical sciences Methacrylates - pharmacology Microscopy, Electron, Scanning Muscle Contraction - drug effects Muscle, Smooth, Vascular - physiology Nicotine - pharmacology Phentolamine - pharmacology Physostigmine - pharmacology Serotonin - pharmacology Thromboxane A2 - analogs & derivatives Thromboxane A2 - antagonists & inhibitors Thromboxane A2 - pharmacology Thromboxane A2 - physiology Thromboxane-A Synthase - antagonists & inhibitors Tobacco, tobacco smoking Toxicology |
title | Endothelium-dependent contraction induced by nicotine in isolated canine basilar artery -possible involvement of a thromboxane A2 (TXA2) like substance |
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