Knock-Out of the Potassium Channel TASK-1 Leads to a Prolonged QT Interval and a Disturbed QRS Complex
Background/Aims: The aim of the study was to characterize the whole cell current of the two-pore domain potassium channel TASK-1 (K2P3) in mouse ventricular cardiomyocytes (I TASK-1 ) and to analyze the cardiac phenotype of the TASK-1 -/- mice. Methods and Results: We have quantified the ventricular...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2011-01, Vol.28 (1), p.77-86 |
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| creator | Decher, Niels Wemhöner, Konstantin Rinné, Susanne Netter, Michael F. Zuzarte, Marylou Aller, Maria I. Kaufmann, Susann G. Li, Xian Tao Meuth, Sven G. Daut, Jürgen Sachse, Frank B. Maier, Sebastian K.G. |
| description | Background/Aims: The aim of the study was to characterize the whole cell current of the two-pore domain potassium channel TASK-1 (K2P3) in mouse ventricular cardiomyocytes (I TASK-1 ) and to analyze the cardiac phenotype of the TASK-1 -/- mice. Methods and Results: We have quantified the ventricular I TASK-1 current using the blocker A293 and TASK-1 -/- mice. Surface electrocardiogram recordings of TASK-1 -/- mice showed a prolonged QTc interval and a broadened QRS complex. The differences in electrocardiograms between wild type and TASK-1 -/- mice disappeared during sympathetic stimulation of the animals. Quantitative RT-PCR, patch clamp recordings and measurements of hemodynamic performance of TASK-1 -/- mice revealed no major compensatory changes in ion channel transcription. Action potential recordings of TASK-1 -/- mouse cardiomyocytes indicated that I TASK-1 modulates action potential duration. Our in vivo electrophysiological studies showed that isoflurane, which activates TASK-1, slowed heart rate and atrioventricular conduction of wild-type but not of TASK-1 -/- mice. Conclusion: The results of an invasive electrophysiological catheter protocol in combination with the observed QRS time prolongation in the surface electrocardiogram point towards a regulatory role of TASK-1 in the cardiac conduction system. |
| doi_str_mv | 10.1159/000331715 |
| format | Article |
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Methods and Results: We have quantified the ventricular I TASK-1 current using the blocker A293 and TASK-1 -/- mice. Surface electrocardiogram recordings of TASK-1 -/- mice showed a prolonged QTc interval and a broadened QRS complex. The differences in electrocardiograms between wild type and TASK-1 -/- mice disappeared during sympathetic stimulation of the animals. Quantitative RT-PCR, patch clamp recordings and measurements of hemodynamic performance of TASK-1 -/- mice revealed no major compensatory changes in ion channel transcription. Action potential recordings of TASK-1 -/- mouse cardiomyocytes indicated that I TASK-1 modulates action potential duration. Our in vivo electrophysiological studies showed that isoflurane, which activates TASK-1, slowed heart rate and atrioventricular conduction of wild-type but not of TASK-1 -/- mice. Conclusion: The results of an invasive electrophysiological catheter protocol in combination with the observed QRS time prolongation in the surface electrocardiogram point towards a regulatory role of TASK-1 in the cardiac conduction system.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000331715</identifier><identifier>PMID: 21865850</identifier><language>eng</language><publisher>Basel, Switzerland</publisher><subject>Action Potentials - physiology ; Anesthetics, Inhalation - pharmacology ; Animals ; Electrophysiological Phenomena - physiology ; Heart Rate - drug effects ; Hemodynamics - physiology ; Isoflurane - pharmacology ; Long QT Syndrome - etiology ; Methoxamine - pharmacology ; Mice ; Mice, Knockout ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - physiology ; Nerve Tissue Proteins - deficiency ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Original Paper ; ortho-Aminobenzoates - pharmacology ; Potassium Channels, Tandem Pore Domain - deficiency ; Potassium Channels, Tandem Pore Domain - genetics ; Potassium Channels, Tandem Pore Domain - metabolism ; Sulfonamides - pharmacology</subject><ispartof>Cellular physiology and biochemistry, 2011-01, Vol.28 (1), p.77-86</ispartof><rights>2011 S. Karger AG, Basel</rights><rights>Copyright © 2011 S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c368t-fe39953479e4a3b138313e59bc4bf73b4ed8d7ce0e240c0fd357adf667f572643</citedby><cites>FETCH-LOGICAL-c368t-fe39953479e4a3b138313e59bc4bf73b4ed8d7ce0e240c0fd357adf667f572643</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21865850$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Decher, Niels</creatorcontrib><creatorcontrib>Wemhöner, Konstantin</creatorcontrib><creatorcontrib>Rinné, Susanne</creatorcontrib><creatorcontrib>Netter, Michael F.</creatorcontrib><creatorcontrib>Zuzarte, Marylou</creatorcontrib><creatorcontrib>Aller, Maria I.</creatorcontrib><creatorcontrib>Kaufmann, Susann G.</creatorcontrib><creatorcontrib>Li, Xian Tao</creatorcontrib><creatorcontrib>Meuth, Sven G.</creatorcontrib><creatorcontrib>Daut, Jürgen</creatorcontrib><creatorcontrib>Sachse, Frank B.</creatorcontrib><creatorcontrib>Maier, Sebastian K.G.</creatorcontrib><title>Knock-Out of the Potassium Channel TASK-1 Leads to a Prolonged QT Interval and a Disturbed QRS Complex</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: The aim of the study was to characterize the whole cell current of the two-pore domain potassium channel TASK-1 (K2P3) in mouse ventricular cardiomyocytes (I TASK-1 ) and to analyze the cardiac phenotype of the TASK-1 -/- mice. Methods and Results: We have quantified the ventricular I TASK-1 current using the blocker A293 and TASK-1 -/- mice. Surface electrocardiogram recordings of TASK-1 -/- mice showed a prolonged QTc interval and a broadened QRS complex. The differences in electrocardiograms between wild type and TASK-1 -/- mice disappeared during sympathetic stimulation of the animals. Quantitative RT-PCR, patch clamp recordings and measurements of hemodynamic performance of TASK-1 -/- mice revealed no major compensatory changes in ion channel transcription. Action potential recordings of TASK-1 -/- mouse cardiomyocytes indicated that I TASK-1 modulates action potential duration. Our in vivo electrophysiological studies showed that isoflurane, which activates TASK-1, slowed heart rate and atrioventricular conduction of wild-type but not of TASK-1 -/- mice. Conclusion: The results of an invasive electrophysiological catheter protocol in combination with the observed QRS time prolongation in the surface electrocardiogram point towards a regulatory role of TASK-1 in the cardiac conduction system.</description><subject>Action Potentials - physiology</subject><subject>Anesthetics, Inhalation - pharmacology</subject><subject>Animals</subject><subject>Electrophysiological Phenomena - physiology</subject><subject>Heart Rate - drug effects</subject><subject>Hemodynamics - physiology</subject><subject>Isoflurane - pharmacology</subject><subject>Long QT Syndrome - etiology</subject><subject>Methoxamine - pharmacology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - physiology</subject><subject>Nerve Tissue Proteins - deficiency</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Original Paper</subject><subject>ortho-Aminobenzoates - pharmacology</subject><subject>Potassium Channels, Tandem Pore Domain - deficiency</subject><subject>Potassium Channels, Tandem Pore Domain - genetics</subject><subject>Potassium Channels, Tandem Pore Domain - metabolism</subject><subject>Sulfonamides - pharmacology</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpt0DtPwzAUBWALgXgUBnaELDEghoAdx7E9lvCqWokCZY6c-BoKSVzsBMG_J6ilE9P11fl8h4PQISXnlHJ1QQhhjArKN9AuTWIaKSHkZv8mlEdSSbGD9kJ4I_0qVLyNdmIqUy452UV23LjyPbrvWuwsbl8BT12rQ5h3Nc5eddNAhWfDp3FE8QS0Cbh1WOOpd5VrXsDghxkeNS34T11h3Zg-u5qHtvPFb_b4hDNXLyr42kdbVlcBDlZzgJ5vrmfZXTS5vx1lw0lUslS2kQWmFGeJUJBoVlAmGWXAVVEmhRWsSMBII0ogECekJNYwLrSxaSosF3GasAE6Xd5dePfRQWjzeh5KqCrdgOtCLiXnXAka9_JsKUvvQvBg84Wf19p_55Tkv63m61Z7e7y62hU1mLX8q7EHR0vwrv0L-DVY_z_5N86ml0uRL4xlP9PshJ4</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Decher, Niels</creator><creator>Wemhöner, Konstantin</creator><creator>Rinné, Susanne</creator><creator>Netter, Michael F.</creator><creator>Zuzarte, Marylou</creator><creator>Aller, Maria I.</creator><creator>Kaufmann, Susann G.</creator><creator>Li, Xian Tao</creator><creator>Meuth, Sven G.</creator><creator>Daut, Jürgen</creator><creator>Sachse, Frank B.</creator><creator>Maier, Sebastian K.G.</creator><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>20110101</creationdate><title>Knock-Out of the Potassium Channel TASK-1 Leads to a Prolonged QT Interval and a Disturbed QRS Complex</title><author>Decher, Niels ; Wemhöner, Konstantin ; Rinné, Susanne ; Netter, Michael F. ; Zuzarte, Marylou ; Aller, Maria I. ; Kaufmann, Susann G. ; Li, Xian Tao ; Meuth, Sven G. ; Daut, Jürgen ; Sachse, Frank B. ; Maier, Sebastian K.G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c368t-fe39953479e4a3b138313e59bc4bf73b4ed8d7ce0e240c0fd357adf667f572643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Action Potentials - physiology</topic><topic>Anesthetics, Inhalation - pharmacology</topic><topic>Animals</topic><topic>Electrophysiological Phenomena - physiology</topic><topic>Heart Rate - drug effects</topic><topic>Hemodynamics - physiology</topic><topic>Isoflurane - pharmacology</topic><topic>Long QT Syndrome - etiology</topic><topic>Methoxamine - pharmacology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - physiology</topic><topic>Nerve Tissue Proteins - deficiency</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Original Paper</topic><topic>ortho-Aminobenzoates - pharmacology</topic><topic>Potassium Channels, Tandem Pore Domain - deficiency</topic><topic>Potassium Channels, Tandem Pore Domain - genetics</topic><topic>Potassium Channels, Tandem Pore Domain - metabolism</topic><topic>Sulfonamides - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Decher, Niels</creatorcontrib><creatorcontrib>Wemhöner, Konstantin</creatorcontrib><creatorcontrib>Rinné, Susanne</creatorcontrib><creatorcontrib>Netter, Michael F.</creatorcontrib><creatorcontrib>Zuzarte, Marylou</creatorcontrib><creatorcontrib>Aller, Maria I.</creatorcontrib><creatorcontrib>Kaufmann, Susann G.</creatorcontrib><creatorcontrib>Li, Xian Tao</creatorcontrib><creatorcontrib>Meuth, Sven G.</creatorcontrib><creatorcontrib>Daut, Jürgen</creatorcontrib><creatorcontrib>Sachse, Frank B.</creatorcontrib><creatorcontrib>Maier, Sebastian K.G.</creatorcontrib><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>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Decher, Niels</au><au>Wemhöner, Konstantin</au><au>Rinné, Susanne</au><au>Netter, Michael F.</au><au>Zuzarte, Marylou</au><au>Aller, Maria I.</au><au>Kaufmann, Susann G.</au><au>Li, Xian Tao</au><au>Meuth, Sven G.</au><au>Daut, Jürgen</au><au>Sachse, Frank B.</au><au>Maier, Sebastian K.G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Knock-Out of the Potassium Channel TASK-1 Leads to a Prolonged QT Interval and a Disturbed QRS Complex</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>28</volume><issue>1</issue><spage>77</spage><epage>86</epage><pages>77-86</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: The aim of the study was to characterize the whole cell current of the two-pore domain potassium channel TASK-1 (K2P3) in mouse ventricular cardiomyocytes (I TASK-1 ) and to analyze the cardiac phenotype of the TASK-1 -/- mice. Methods and Results: We have quantified the ventricular I TASK-1 current using the blocker A293 and TASK-1 -/- mice. Surface electrocardiogram recordings of TASK-1 -/- mice showed a prolonged QTc interval and a broadened QRS complex. The differences in electrocardiograms between wild type and TASK-1 -/- mice disappeared during sympathetic stimulation of the animals. Quantitative RT-PCR, patch clamp recordings and measurements of hemodynamic performance of TASK-1 -/- mice revealed no major compensatory changes in ion channel transcription. Action potential recordings of TASK-1 -/- mouse cardiomyocytes indicated that I TASK-1 modulates action potential duration. Our in vivo electrophysiological studies showed that isoflurane, which activates TASK-1, slowed heart rate and atrioventricular conduction of wild-type but not of TASK-1 -/- mice. Conclusion: The results of an invasive electrophysiological catheter protocol in combination with the observed QRS time prolongation in the surface electrocardiogram point towards a regulatory role of TASK-1 in the cardiac conduction system.</abstract><cop>Basel, Switzerland</cop><pmid>21865850</pmid><doi>10.1159/000331715</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Action Potentials - physiology Anesthetics, Inhalation - pharmacology Animals Electrophysiological Phenomena - physiology Heart Rate - drug effects Hemodynamics - physiology Isoflurane - pharmacology Long QT Syndrome - etiology Methoxamine - pharmacology Mice Mice, Knockout Myocytes, Cardiac - drug effects Myocytes, Cardiac - physiology Nerve Tissue Proteins - deficiency Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Original Paper ortho-Aminobenzoates - pharmacology Potassium Channels, Tandem Pore Domain - deficiency Potassium Channels, Tandem Pore Domain - genetics Potassium Channels, Tandem Pore Domain - metabolism Sulfonamides - pharmacology |
| title | Knock-Out of the Potassium Channel TASK-1 Leads to a Prolonged QT Interval and a Disturbed QRS Complex |
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