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Comparison of the pharmacological properties of EDHF‐mediated vasorelaxation in guinea‐pig cerebral and mesenteric resistance vessels
In the presence of L‐NNA (100 μM), indomethacin (10 μM) and ODQ (10 μM), acetylcholine induced a concentration‐dependent vasorelaxation of guinea‐pig mesenteric and middle cerebral arteries precontracted with cirazoline or histamine, but not with high K+, indicating the contribution of an endotheliu...
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| Published in: | British journal of pharmacology 2000-08, Vol.130 (8), p.1983-1991 |
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| container_end_page | 1991 |
| container_issue | 8 |
| container_start_page | 1983 |
| container_title | British journal of pharmacology |
| container_volume | 130 |
| creator | Dong, Hui Jiang, Yanfen Cole, William C Triggle, Christopher R |
| description | In the presence of L‐NNA (100 μM), indomethacin (10 μM) and ODQ (10 μM), acetylcholine induced a concentration‐dependent vasorelaxation of guinea‐pig mesenteric and middle cerebral arteries precontracted with cirazoline or histamine, but not with high K+, indicating the contribution of an endothelium‐derived hyperpolarizing factor (EDHF).
In cerebral arteries, charybdotoxin (ChTX; 0.1 μM) completely inhibited the indomethacin, L‐NNA and ODQ‐insensitive relaxation; iberiotoxin (IbTX, 0.1 μM), 4‐aminopyridine (4‐AP, 1 mM), or barium (30 μM) significantly reduced the response; in the mesenteric artery, ChTX and IbTX also reduced this relaxation. Glibenclamide (10 μM) had no affect in either the mesenteric or cerebral artery.
Neither clotrimazole (1 μM) nor 7‐ethoxyresorufin (3 μM) affected EDHF‐mediated relaxation in the mesenteric artery, but abolished or attenuated EDHF‐mediated relaxations in the cerebral artery. AM404 (30 μM), a selective anandamide transport inhibitor, did not affect the vasorelaxation response to acetylcholine in the cerebral artery, but in the mesenteric artery potentiated the vasorelaxation response to acetylcholine in an IbTX, and apamin‐sensitive, but SR 141816A‐insensitive manner. Ouabain (100 μM) almost abolished EDHF‐mediated relaxation in the mesenteric artery, but enhanced the relaxation in the cerebral artery whereas the addition of K+ (5–20 mM) to precontracted guinea‐pig cerebral or mesenteric artery induced further vasoconstriction.
These data suggest that in the guinea‐pig mesenteric and cerebral arteries different EDHFs mediate acetylcholine‐induced relaxation, however, EDHF is unlikely to be mediated by K+.
British Journal of Pharmacology (2000) 130, 1983–1991; doi:10.1038/sj.bjp.0703474 |
| doi_str_mv | 10.1038/sj.bjp.0703474 |
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In cerebral arteries, charybdotoxin (ChTX; 0.1 μM) completely inhibited the indomethacin, L‐NNA and ODQ‐insensitive relaxation; iberiotoxin (IbTX, 0.1 μM), 4‐aminopyridine (4‐AP, 1 mM), or barium (30 μM) significantly reduced the response; in the mesenteric artery, ChTX and IbTX also reduced this relaxation. Glibenclamide (10 μM) had no affect in either the mesenteric or cerebral artery.
Neither clotrimazole (1 μM) nor 7‐ethoxyresorufin (3 μM) affected EDHF‐mediated relaxation in the mesenteric artery, but abolished or attenuated EDHF‐mediated relaxations in the cerebral artery. AM404 (30 μM), a selective anandamide transport inhibitor, did not affect the vasorelaxation response to acetylcholine in the cerebral artery, but in the mesenteric artery potentiated the vasorelaxation response to acetylcholine in an IbTX, and apamin‐sensitive, but SR 141816A‐insensitive manner. Ouabain (100 μM) almost abolished EDHF‐mediated relaxation in the mesenteric artery, but enhanced the relaxation in the cerebral artery whereas the addition of K+ (5–20 mM) to precontracted guinea‐pig cerebral or mesenteric artery induced further vasoconstriction.
These data suggest that in the guinea‐pig mesenteric and cerebral arteries different EDHFs mediate acetylcholine‐induced relaxation, however, EDHF is unlikely to be mediated by K+.
British Journal of Pharmacology (2000) 130, 1983–1991; doi:10.1038/sj.bjp.0703474</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0703474</identifier><identifier>PMID: 10952691</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>4-Aminopyridine - pharmacology ; Acetylcholine ; Acetylcholine - pharmacology ; Anandamide ; Animals ; Arachidonic Acids - pharmacology ; Barium ; Biological and medical sciences ; Biological Factors - physiology ; calcium‐activated potassium channels ; Cell physiology ; Cerebral Arteries - drug effects ; Cerebral Arteries - physiology ; Charybdotoxin ; Charybdotoxin - pharmacology ; Clotrimazole ; Cytochrome P-450 Enzyme System - metabolism ; cytochrome P450 ; Data processing ; delayed rectifier potassium channels ; Dose-Response Relationship, Drug ; Endothelium, Vascular - physiology ; endothelium‐derived hyperpolarizing factor (EDHF) ; Enzyme Inhibitors - pharmacology ; Fundamental and applied biological sciences. Psychology ; glibenclamide ; Glyburide - pharmacology ; Guinea Pigs ; Histamine ; Imidazoles - pharmacology ; In Vitro Techniques ; Indomethacin ; Indomethacin - pharmacology ; inwardly rectifying potassium channels ; Male ; Mesenteric Arteries - drug effects ; Mesenteric Arteries - physiology ; mesenteric artery ; middle cerebral artery ; Molecular and cellular biology ; Muscle contraction ; Nitric Oxide - physiology ; Nitroarginine - pharmacology ; Ouabain ; Ouabain - pharmacology ; Oxadiazoles - pharmacology ; Pharmacology ; Potassium ; Potassium Channel Blockers ; Potassium Channels - physiology ; Quinoxalines - pharmacology ; Vasodilation ; Vasodilation - drug effects ; Vasodilator Agents - pharmacology</subject><ispartof>British journal of pharmacology, 2000-08, Vol.130 (8), p.1983-1991</ispartof><rights>2000 British Pharmacological Society</rights><rights>2000 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Aug 2000</rights><rights>Copyright 2000, Nature Publishing Group 2000 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5851-e62dcf1a2fc5bba19d99c3a0f84ecc5823f79cd0ff9dcfa49deae6f679ca88073</citedby><cites>FETCH-LOGICAL-c5851-e62dcf1a2fc5bba19d99c3a0f84ecc5823f79cd0ff9dcfa49deae6f679ca88073</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1038%2Fsj.bjp.0703474$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1038%2Fsj.bjp.0703474$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,733,786,790,891,1424,27957,27958,45609,45610,50923,51032,53827,53829</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1481784$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10952691$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dong, Hui</creatorcontrib><creatorcontrib>Jiang, Yanfen</creatorcontrib><creatorcontrib>Cole, William C</creatorcontrib><creatorcontrib>Triggle, Christopher R</creatorcontrib><title>Comparison of the pharmacological properties of EDHF‐mediated vasorelaxation in guinea‐pig cerebral and mesenteric resistance vessels</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>In the presence of L‐NNA (100 μM), indomethacin (10 μM) and ODQ (10 μM), acetylcholine induced a concentration‐dependent vasorelaxation of guinea‐pig mesenteric and middle cerebral arteries precontracted with cirazoline or histamine, but not with high K+, indicating the contribution of an endothelium‐derived hyperpolarizing factor (EDHF).
In cerebral arteries, charybdotoxin (ChTX; 0.1 μM) completely inhibited the indomethacin, L‐NNA and ODQ‐insensitive relaxation; iberiotoxin (IbTX, 0.1 μM), 4‐aminopyridine (4‐AP, 1 mM), or barium (30 μM) significantly reduced the response; in the mesenteric artery, ChTX and IbTX also reduced this relaxation. Glibenclamide (10 μM) had no affect in either the mesenteric or cerebral artery.
Neither clotrimazole (1 μM) nor 7‐ethoxyresorufin (3 μM) affected EDHF‐mediated relaxation in the mesenteric artery, but abolished or attenuated EDHF‐mediated relaxations in the cerebral artery. AM404 (30 μM), a selective anandamide transport inhibitor, did not affect the vasorelaxation response to acetylcholine in the cerebral artery, but in the mesenteric artery potentiated the vasorelaxation response to acetylcholine in an IbTX, and apamin‐sensitive, but SR 141816A‐insensitive manner. Ouabain (100 μM) almost abolished EDHF‐mediated relaxation in the mesenteric artery, but enhanced the relaxation in the cerebral artery whereas the addition of K+ (5–20 mM) to precontracted guinea‐pig cerebral or mesenteric artery induced further vasoconstriction.
These data suggest that in the guinea‐pig mesenteric and cerebral arteries different EDHFs mediate acetylcholine‐induced relaxation, however, EDHF is unlikely to be mediated by K+.
British Journal of Pharmacology (2000) 130, 1983–1991; doi:10.1038/sj.bjp.0703474</description><subject>4-Aminopyridine - pharmacology</subject><subject>Acetylcholine</subject><subject>Acetylcholine - pharmacology</subject><subject>Anandamide</subject><subject>Animals</subject><subject>Arachidonic Acids - pharmacology</subject><subject>Barium</subject><subject>Biological and medical sciences</subject><subject>Biological Factors - physiology</subject><subject>calcium‐activated potassium channels</subject><subject>Cell physiology</subject><subject>Cerebral Arteries - drug effects</subject><subject>Cerebral Arteries - physiology</subject><subject>Charybdotoxin</subject><subject>Charybdotoxin - pharmacology</subject><subject>Clotrimazole</subject><subject>Cytochrome P-450 Enzyme System - metabolism</subject><subject>cytochrome P450</subject><subject>Data processing</subject><subject>delayed rectifier potassium channels</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelium, Vascular - physiology</subject><subject>endothelium‐derived hyperpolarizing factor (EDHF)</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>glibenclamide</subject><subject>Glyburide - pharmacology</subject><subject>Guinea Pigs</subject><subject>Histamine</subject><subject>Imidazoles - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Indomethacin</subject><subject>Indomethacin - pharmacology</subject><subject>inwardly rectifying potassium channels</subject><subject>Male</subject><subject>Mesenteric Arteries - drug effects</subject><subject>Mesenteric Arteries - physiology</subject><subject>mesenteric artery</subject><subject>middle cerebral artery</subject><subject>Molecular and cellular biology</subject><subject>Muscle contraction</subject><subject>Nitric Oxide - physiology</subject><subject>Nitroarginine - pharmacology</subject><subject>Ouabain</subject><subject>Ouabain - pharmacology</subject><subject>Oxadiazoles - pharmacology</subject><subject>Pharmacology</subject><subject>Potassium</subject><subject>Potassium Channel Blockers</subject><subject>Potassium Channels - physiology</subject><subject>Quinoxalines - pharmacology</subject><subject>Vasodilation</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNqFkT-P1DAQxSME4paDlhJZiIImiyf_0yDBcscinQQF1NbEGe96lcTBkyxcR0t3n_E-CV7tCg4aKkuen9-85xdFT0EuQabVK94tm924lKVMszK7Fy0gK4s4Tyu4Hy2klGUMUFVn0SPmnZRhWOYPozOQdZ4UNSyinyvXj-gtu0E4I6YtiXGLvkftOrexGjsxejeSnyzxgbh4t768_XHTU2txolbskZ2nDr_jZIOGHcRmtgNhYEa7EZo8NT6o4NCKnpiGibzVwhNbnnDQJPbETB0_jh4Y7JienM7z6MvlxefVOr76-P7D6s1VrPMqh5iKpNUGMDE6bxqEuq1rnaI0VUY6IElqylq30pg6cJjVLSEVpgiXWFWyTM-j10fdcW5CCh0cBX9q9LZHf60cWvX3ZLBbtXF7BXmZJLkMAi9PAt59nYkn1VvW1HU4kJtZgUzCniLLioA-_wfdudkPIZ5KoIQaijwL0PIIae-YPZnfXkCqQ8mKdyqUrE4lhwfP7ia4gx9bDcCLE4AcGjQ-_LPlP1xWQVkddNIj9s12dP2frertpzUUAOkvSTTHig</recordid><startdate>200008</startdate><enddate>200008</enddate><creator>Dong, Hui</creator><creator>Jiang, Yanfen</creator><creator>Cole, William C</creator><creator>Triggle, Christopher R</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>200008</creationdate><title>Comparison of the pharmacological properties of EDHF‐mediated vasorelaxation in guinea‐pig cerebral and mesenteric resistance vessels</title><author>Dong, Hui ; Jiang, Yanfen ; Cole, William C ; Triggle, Christopher R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5851-e62dcf1a2fc5bba19d99c3a0f84ecc5823f79cd0ff9dcfa49deae6f679ca88073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>4-Aminopyridine - pharmacology</topic><topic>Acetylcholine</topic><topic>Acetylcholine - pharmacology</topic><topic>Anandamide</topic><topic>Animals</topic><topic>Arachidonic Acids - pharmacology</topic><topic>Barium</topic><topic>Biological and medical sciences</topic><topic>Biological Factors - physiology</topic><topic>calcium‐activated potassium channels</topic><topic>Cell physiology</topic><topic>Cerebral Arteries - drug effects</topic><topic>Cerebral Arteries - physiology</topic><topic>Charybdotoxin</topic><topic>Charybdotoxin - pharmacology</topic><topic>Clotrimazole</topic><topic>Cytochrome P-450 Enzyme System - metabolism</topic><topic>cytochrome P450</topic><topic>Data processing</topic><topic>delayed rectifier potassium channels</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelium, Vascular - physiology</topic><topic>endothelium‐derived hyperpolarizing factor (EDHF)</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>glibenclamide</topic><topic>Glyburide - pharmacology</topic><topic>Guinea Pigs</topic><topic>Histamine</topic><topic>Imidazoles - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Indomethacin</topic><topic>Indomethacin - pharmacology</topic><topic>inwardly rectifying potassium channels</topic><topic>Male</topic><topic>Mesenteric Arteries - drug effects</topic><topic>Mesenteric Arteries - physiology</topic><topic>mesenteric artery</topic><topic>middle cerebral artery</topic><topic>Molecular and cellular biology</topic><topic>Muscle contraction</topic><topic>Nitric Oxide - physiology</topic><topic>Nitroarginine - pharmacology</topic><topic>Ouabain</topic><topic>Ouabain - pharmacology</topic><topic>Oxadiazoles - pharmacology</topic><topic>Pharmacology</topic><topic>Potassium</topic><topic>Potassium Channel Blockers</topic><topic>Potassium Channels - physiology</topic><topic>Quinoxalines - pharmacology</topic><topic>Vasodilation</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dong, Hui</creatorcontrib><creatorcontrib>Jiang, Yanfen</creatorcontrib><creatorcontrib>Cole, William C</creatorcontrib><creatorcontrib>Triggle, Christopher R</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Complete (ProQuest Database)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</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>Dong, Hui</au><au>Jiang, Yanfen</au><au>Cole, William C</au><au>Triggle, Christopher R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comparison of the pharmacological properties of EDHF‐mediated vasorelaxation in guinea‐pig cerebral and mesenteric resistance vessels</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2000-08</date><risdate>2000</risdate><volume>130</volume><issue>8</issue><spage>1983</spage><epage>1991</epage><pages>1983-1991</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><abstract>In the presence of L‐NNA (100 μM), indomethacin (10 μM) and ODQ (10 μM), acetylcholine induced a concentration‐dependent vasorelaxation of guinea‐pig mesenteric and middle cerebral arteries precontracted with cirazoline or histamine, but not with high K+, indicating the contribution of an endothelium‐derived hyperpolarizing factor (EDHF).
In cerebral arteries, charybdotoxin (ChTX; 0.1 μM) completely inhibited the indomethacin, L‐NNA and ODQ‐insensitive relaxation; iberiotoxin (IbTX, 0.1 μM), 4‐aminopyridine (4‐AP, 1 mM), or barium (30 μM) significantly reduced the response; in the mesenteric artery, ChTX and IbTX also reduced this relaxation. Glibenclamide (10 μM) had no affect in either the mesenteric or cerebral artery.
Neither clotrimazole (1 μM) nor 7‐ethoxyresorufin (3 μM) affected EDHF‐mediated relaxation in the mesenteric artery, but abolished or attenuated EDHF‐mediated relaxations in the cerebral artery. AM404 (30 μM), a selective anandamide transport inhibitor, did not affect the vasorelaxation response to acetylcholine in the cerebral artery, but in the mesenteric artery potentiated the vasorelaxation response to acetylcholine in an IbTX, and apamin‐sensitive, but SR 141816A‐insensitive manner. Ouabain (100 μM) almost abolished EDHF‐mediated relaxation in the mesenteric artery, but enhanced the relaxation in the cerebral artery whereas the addition of K+ (5–20 mM) to precontracted guinea‐pig cerebral or mesenteric artery induced further vasoconstriction.
These data suggest that in the guinea‐pig mesenteric and cerebral arteries different EDHFs mediate acetylcholine‐induced relaxation, however, EDHF is unlikely to be mediated by K+.
British Journal of Pharmacology (2000) 130, 1983–1991; doi:10.1038/sj.bjp.0703474</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10952691</pmid><doi>10.1038/sj.bjp.0703474</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0007-1188 |
| ispartof | British journal of pharmacology, 2000-08, Vol.130 (8), p.1983-1991 |
| issn | 0007-1188 1476-5381 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1572250 |
| source | Open Access: PubMed Central; Wiley Online Library |
| subjects | 4-Aminopyridine - pharmacology Acetylcholine Acetylcholine - pharmacology Anandamide Animals Arachidonic Acids - pharmacology Barium Biological and medical sciences Biological Factors - physiology calcium‐activated potassium channels Cell physiology Cerebral Arteries - drug effects Cerebral Arteries - physiology Charybdotoxin Charybdotoxin - pharmacology Clotrimazole Cytochrome P-450 Enzyme System - metabolism cytochrome P450 Data processing delayed rectifier potassium channels Dose-Response Relationship, Drug Endothelium, Vascular - physiology endothelium‐derived hyperpolarizing factor (EDHF) Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology glibenclamide Glyburide - pharmacology Guinea Pigs Histamine Imidazoles - pharmacology In Vitro Techniques Indomethacin Indomethacin - pharmacology inwardly rectifying potassium channels Male Mesenteric Arteries - drug effects Mesenteric Arteries - physiology mesenteric artery middle cerebral artery Molecular and cellular biology Muscle contraction Nitric Oxide - physiology Nitroarginine - pharmacology Ouabain Ouabain - pharmacology Oxadiazoles - pharmacology Pharmacology Potassium Potassium Channel Blockers Potassium Channels - physiology Quinoxalines - pharmacology Vasodilation Vasodilation - drug effects Vasodilator Agents - pharmacology |
| title | Comparison of the pharmacological properties of EDHF‐mediated vasorelaxation in guinea‐pig cerebral and mesenteric resistance vessels |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-22T00%3A32%3A11IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Comparison%20of%20the%20pharmacological%20properties%20of%20EDHF%E2%80%90mediated%20vasorelaxation%20in%20guinea%E2%80%90pig%20cerebral%20and%20mesenteric%20resistance%20vessels&rft.jtitle=British%20journal%20of%20pharmacology&rft.au=Dong,%20Hui&rft.date=2000-08&rft.volume=130&rft.issue=8&rft.spage=1983&rft.epage=1991&rft.pages=1983-1991&rft.issn=0007-1188&rft.eissn=1476-5381&rft.coden=BJPCBM&rft_id=info:doi/10.1038/sj.bjp.0703474&rft_dat=%3Cproquest_pubme%3E1028399361%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c5851-e62dcf1a2fc5bba19d99c3a0f84ecc5823f79cd0ff9dcfa49deae6f679ca88073%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=217191654&rft_id=info:pmid/10952691&rfr_iscdi=true |