Role of endothelial cell hyperpolarization in EDHF‐mediated responses in the guinea‐pig carotid artery
Experiments were performed to identify the potassium channels involved in the acetylcholine‐induced endothelium‐dependent hyperpolarization of the guinea‐pig internal carotid artery. Smooth muscle and endothelial cell membrane potentials were recorded in isolated arteries with intracellular microele...
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| creator | Quignard, J ‐F Félétou, M Edwards, G Duhault, J Weston, A H Vanhoutte, P M |
| description | Experiments were performed to identify the potassium channels involved in the acetylcholine‐induced endothelium‐dependent hyperpolarization of the guinea‐pig internal carotid artery. Smooth muscle and endothelial cell membrane potentials were recorded in isolated arteries with intracellular microelectrodes. Potassium currents were recorded in freshly‐dissociated smooth muscle cells using patch clamp techniques.
In single myocytes, iberiotoxin (0.1 μM)‐, charybdotoxin (0.1 μM)‐, apamin (0.5 μM)‐ and 4‐aminopyridine (5 mM)‐sensitive potassium currents were identified indicating the presence of large‐ and small‐conductance calcium‐sensitive potassium channels (BKCa and SKCa) as well as voltage‐dependent potassium channels (KV). Charybdotoxin and iberiotoxin inhibited the same population of BKCa but a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected. 4‐aminopyridine (0.1–25 mM) induced a concentration‐dependent inhibition of KV without affecting the iberiotoxin‐ or the apamin‐sensitive currents.
In isolated arteries, both the endothelium‐dependent hyperpolarization of smooth muscle and the hyperpolarization of endothelial cells induced by acetylcholine or by substance P were inhibited by 5 mM 4‐aminopyridine.
These results indicate that in the vascular smooth muscle cells of the guinea‐pig carotid artery, a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected, comforting the hypothesis that the combination of these two toxins should act on the endothelial cells. Furthermore, the inhibition by 4‐aminopyridine of both smooth muscle and endothelial hyperpolarizations, suggests that in order to observe an endothelium‐dependent hyperpolarization of the vascular smooth muscle cells, the activation of endothelial potassium channels is likely to be required.
British Journal of Pharmacology (2000) 129, 1103–1112; doi:10.1038/sj.bjp.0703175 |
| doi_str_mv | 10.1038/sj.bjp.0703175 |
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In single myocytes, iberiotoxin (0.1 μM)‐, charybdotoxin (0.1 μM)‐, apamin (0.5 μM)‐ and 4‐aminopyridine (5 mM)‐sensitive potassium currents were identified indicating the presence of large‐ and small‐conductance calcium‐sensitive potassium channels (BKCa and SKCa) as well as voltage‐dependent potassium channels (KV). Charybdotoxin and iberiotoxin inhibited the same population of BKCa but a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected. 4‐aminopyridine (0.1–25 mM) induced a concentration‐dependent inhibition of KV without affecting the iberiotoxin‐ or the apamin‐sensitive currents.
In isolated arteries, both the endothelium‐dependent hyperpolarization of smooth muscle and the hyperpolarization of endothelial cells induced by acetylcholine or by substance P were inhibited by 5 mM 4‐aminopyridine.
These results indicate that in the vascular smooth muscle cells of the guinea‐pig carotid artery, a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected, comforting the hypothesis that the combination of these two toxins should act on the endothelial cells. Furthermore, the inhibition by 4‐aminopyridine of both smooth muscle and endothelial hyperpolarizations, suggests that in order to observe an endothelium‐dependent hyperpolarization of the vascular smooth muscle cells, the activation of endothelial potassium channels is likely to be required.
British Journal of Pharmacology (2000) 129, 1103–1112; doi:10.1038/sj.bjp.0703175</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0703175</identifier><identifier>PMID: 10725258</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>4-Aminopyridine - pharmacology ; 4‐Aminopyridine ; Acetylcholine - pharmacology ; Animals ; apamin ; Biological and medical sciences ; Biological Factors - antagonists & inhibitors ; Biological Factors - pharmacology ; Calcium - metabolism ; Cardiovascular system ; Carotid Arteries - drug effects ; Cell Membrane - drug effects ; Cell Membrane - physiology ; Cell membranes. Ionic channels. Membrane pores ; Cell structures and functions ; charybdotoxin ; EDHF ; Electrophysiology ; endothelium ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Fundamental and applied biological sciences. Psychology ; Guinea Pigs ; iberiotoxin ; In Vitro Techniques ; Male ; Medical sciences ; Membrane Potentials - physiology ; Microelectrodes ; Miscellaneous ; Molecular and cellular biology ; Muscle, Smooth, Vascular - drug effects ; Patch-Clamp Techniques ; Peptides - pharmacology ; Pharmacology. Drug treatments ; Potassium Channel Blockers ; potassium channels ; Potassium Channels - drug effects ; smooth muscle ; Substance P - pharmacology</subject><ispartof>British journal of pharmacology, 2000-03, Vol.129 (6), p.1103-1112</ispartof><rights>2000 British Pharmacological Society</rights><rights>2000 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Mar 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-c5523-7650a73032e2621686be5093c3cd777281168f22d787dcf39a39f3f1ab5d7df13</citedby><cites>FETCH-LOGICAL-c5523-7650a73032e2621686be5093c3cd777281168f22d787dcf39a39f3f1ab5d7df13</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/PMC1571951/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1571951/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,1418,1434,27929,27930,45579,45580,46414,46838,53796,53798</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1298090$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10725258$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Quignard, J ‐F</creatorcontrib><creatorcontrib>Félétou, M</creatorcontrib><creatorcontrib>Edwards, G</creatorcontrib><creatorcontrib>Duhault, J</creatorcontrib><creatorcontrib>Weston, A H</creatorcontrib><creatorcontrib>Vanhoutte, P M</creatorcontrib><title>Role of endothelial cell hyperpolarization in EDHF‐mediated responses in the guinea‐pig carotid artery</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Experiments were performed to identify the potassium channels involved in the acetylcholine‐induced endothelium‐dependent hyperpolarization of the guinea‐pig internal carotid artery. Smooth muscle and endothelial cell membrane potentials were recorded in isolated arteries with intracellular microelectrodes. Potassium currents were recorded in freshly‐dissociated smooth muscle cells using patch clamp techniques.
In single myocytes, iberiotoxin (0.1 μM)‐, charybdotoxin (0.1 μM)‐, apamin (0.5 μM)‐ and 4‐aminopyridine (5 mM)‐sensitive potassium currents were identified indicating the presence of large‐ and small‐conductance calcium‐sensitive potassium channels (BKCa and SKCa) as well as voltage‐dependent potassium channels (KV). Charybdotoxin and iberiotoxin inhibited the same population of BKCa but a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected. 4‐aminopyridine (0.1–25 mM) induced a concentration‐dependent inhibition of KV without affecting the iberiotoxin‐ or the apamin‐sensitive currents.
In isolated arteries, both the endothelium‐dependent hyperpolarization of smooth muscle and the hyperpolarization of endothelial cells induced by acetylcholine or by substance P were inhibited by 5 mM 4‐aminopyridine.
These results indicate that in the vascular smooth muscle cells of the guinea‐pig carotid artery, a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected, comforting the hypothesis that the combination of these two toxins should act on the endothelial cells. Furthermore, the inhibition by 4‐aminopyridine of both smooth muscle and endothelial hyperpolarizations, suggests that in order to observe an endothelium‐dependent hyperpolarization of the vascular smooth muscle cells, the activation of endothelial potassium channels is likely to be required.
British Journal of Pharmacology (2000) 129, 1103–1112; doi:10.1038/sj.bjp.0703175</description><subject>4-Aminopyridine - pharmacology</subject><subject>4‐Aminopyridine</subject><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>apamin</subject><subject>Biological and medical sciences</subject><subject>Biological Factors - antagonists & inhibitors</subject><subject>Biological Factors - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Cardiovascular system</subject><subject>Carotid Arteries - drug effects</subject><subject>Cell Membrane - drug effects</subject><subject>Cell Membrane - physiology</subject><subject>Cell membranes. Ionic channels. Membrane pores</subject><subject>Cell structures and functions</subject><subject>charybdotoxin</subject><subject>EDHF</subject><subject>Electrophysiology</subject><subject>endothelium</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Guinea Pigs</subject><subject>iberiotoxin</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Potentials - physiology</subject><subject>Microelectrodes</subject><subject>Miscellaneous</subject><subject>Molecular and cellular biology</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Patch-Clamp Techniques</subject><subject>Peptides - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Potassium Channel Blockers</subject><subject>potassium channels</subject><subject>Potassium Channels - drug effects</subject><subject>smooth muscle</subject><subject>Substance P - pharmacology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc2KFDEUhYMoTju6dSlBxF21-ZlUUhthnB9bGFBE1yGdutWdIp2USZXSs_IRfEafxBTd6OjGVSDnuycn9yD0lJIlJVy9yv1y3Q9LIgmnUtxDC3om60pwRe-jBSFEVpQqdYIe5dwTUkQpHqITSiQTTKgF6j9GDzh2GEIbxy14Zzy24D3e7gdIQ_QmuVszuhiwC_jqcnX98_uPHbTOjNDiBHmIIUOexTKON5MLYAoyuA22JsXRtdikEdL-MXrQGZ_hyfE8RZ-vrz5drKqb92_fXZzfVFYIxitZC2IkJ5wBqxmtVb0GQRpuuW2llEzRctcx1kolW9vxxvCm4x01a9HKtqP8FL0--A7TugS1EMZkvB6S25m019E4_bcS3FZv4ldNhaSNmA1eHg1S_DJBHvXO5XknJkCcspakUZywGXz-D9jHKYXyOc1o8SobFgVaHiCbYs4Jut9JKNFzhzr3unSojx2WgWd389_BD6UV4MURMNka3yUTrMt_ONYo0pCC8QP2zXnY_-dV_ebDitdnnP8CUvy4Sw</recordid><startdate>200003</startdate><enddate>200003</enddate><creator>Quignard, J ‐F</creator><creator>Félétou, M</creator><creator>Edwards, G</creator><creator>Duhault, J</creator><creator>Weston, A H</creator><creator>Vanhoutte, P M</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>200003</creationdate><title>Role of endothelial cell hyperpolarization in EDHF‐mediated responses in the guinea‐pig carotid artery</title><author>Quignard, J ‐F ; Félétou, M ; Edwards, G ; Duhault, J ; Weston, A H ; Vanhoutte, P M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5523-7650a73032e2621686be5093c3cd777281168f22d787dcf39a39f3f1ab5d7df13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>4-Aminopyridine - pharmacology</topic><topic>4‐Aminopyridine</topic><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>apamin</topic><topic>Biological and medical sciences</topic><topic>Biological Factors - antagonists & inhibitors</topic><topic>Biological Factors - pharmacology</topic><topic>Calcium - metabolism</topic><topic>Cardiovascular system</topic><topic>Carotid Arteries - drug effects</topic><topic>Cell Membrane - drug effects</topic><topic>Cell Membrane - physiology</topic><topic>Cell membranes. Ionic channels. Membrane pores</topic><topic>Cell structures and functions</topic><topic>charybdotoxin</topic><topic>EDHF</topic><topic>Electrophysiology</topic><topic>endothelium</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Guinea Pigs</topic><topic>iberiotoxin</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Potentials - physiology</topic><topic>Microelectrodes</topic><topic>Miscellaneous</topic><topic>Molecular and cellular biology</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Patch-Clamp Techniques</topic><topic>Peptides - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Potassium Channel Blockers</topic><topic>potassium channels</topic><topic>Potassium Channels - drug effects</topic><topic>smooth muscle</topic><topic>Substance P - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Quignard, J ‐F</creatorcontrib><creatorcontrib>Félétou, M</creatorcontrib><creatorcontrib>Edwards, G</creatorcontrib><creatorcontrib>Duhault, J</creatorcontrib><creatorcontrib>Weston, A H</creatorcontrib><creatorcontrib>Vanhoutte, P 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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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>MEDLINE - Academic</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>Quignard, J ‐F</au><au>Félétou, M</au><au>Edwards, G</au><au>Duhault, J</au><au>Weston, A H</au><au>Vanhoutte, P M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of endothelial cell hyperpolarization in EDHF‐mediated responses in the guinea‐pig carotid artery</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2000-03</date><risdate>2000</risdate><volume>129</volume><issue>6</issue><spage>1103</spage><epage>1112</epage><pages>1103-1112</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Experiments were performed to identify the potassium channels involved in the acetylcholine‐induced endothelium‐dependent hyperpolarization of the guinea‐pig internal carotid artery. Smooth muscle and endothelial cell membrane potentials were recorded in isolated arteries with intracellular microelectrodes. Potassium currents were recorded in freshly‐dissociated smooth muscle cells using patch clamp techniques.
In single myocytes, iberiotoxin (0.1 μM)‐, charybdotoxin (0.1 μM)‐, apamin (0.5 μM)‐ and 4‐aminopyridine (5 mM)‐sensitive potassium currents were identified indicating the presence of large‐ and small‐conductance calcium‐sensitive potassium channels (BKCa and SKCa) as well as voltage‐dependent potassium channels (KV). Charybdotoxin and iberiotoxin inhibited the same population of BKCa but a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected. 4‐aminopyridine (0.1–25 mM) induced a concentration‐dependent inhibition of KV without affecting the iberiotoxin‐ or the apamin‐sensitive currents.
In isolated arteries, both the endothelium‐dependent hyperpolarization of smooth muscle and the hyperpolarization of endothelial cells induced by acetylcholine or by substance P were inhibited by 5 mM 4‐aminopyridine.
These results indicate that in the vascular smooth muscle cells of the guinea‐pig carotid artery, a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected, comforting the hypothesis that the combination of these two toxins should act on the endothelial cells. Furthermore, the inhibition by 4‐aminopyridine of both smooth muscle and endothelial hyperpolarizations, suggests that in order to observe an endothelium‐dependent hyperpolarization of the vascular smooth muscle cells, the activation of endothelial potassium channels is likely to be required.
British Journal of Pharmacology (2000) 129, 1103–1112; doi:10.1038/sj.bjp.0703175</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10725258</pmid><doi>10.1038/sj.bjp.0703175</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 4-Aminopyridine - pharmacology 4‐Aminopyridine Acetylcholine - pharmacology Animals apamin Biological and medical sciences Biological Factors - antagonists & inhibitors Biological Factors - pharmacology Calcium - metabolism Cardiovascular system Carotid Arteries - drug effects Cell Membrane - drug effects Cell Membrane - physiology Cell membranes. Ionic channels. Membrane pores Cell structures and functions charybdotoxin EDHF Electrophysiology endothelium Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - physiology Fundamental and applied biological sciences. Psychology Guinea Pigs iberiotoxin In Vitro Techniques Male Medical sciences Membrane Potentials - physiology Microelectrodes Miscellaneous Molecular and cellular biology Muscle, Smooth, Vascular - drug effects Patch-Clamp Techniques Peptides - pharmacology Pharmacology. Drug treatments Potassium Channel Blockers potassium channels Potassium Channels - drug effects smooth muscle Substance P - pharmacology |
| title | Role of endothelial cell hyperpolarization in EDHF‐mediated responses in the guinea‐pig carotid artery |
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