Targeted G-protein inhibition as a novel approach to decrease vagal atrial fibrillation by selective parasympathetic attenuation
Aims The parasympathetic nervous system is thought to play a key role in atrial fibrillation (AF). Since parasympathetic signalling is primarily mediated by the heterotrimeric G-protein, Gαiβγ, we hypothesized that targeted inhibition of Gαi interactions in the posterior left atrium (PLA) would modi...
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| Veröffentlicht in: | Cardiovascular research 2009-08, Vol.83 (3), p.481-492 |
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| creator | Aistrup, Gary L. Villuendas, Roger Ng, Jason Gilchrist, Annette Lynch, Thomas W. Gordon, David Cokic, Ivan Mottl, Steven Zhou, Rui Dean, David A. Wasserstrom, J. Andrew Goldberger, Jeffrey J. Kadish, Alan H. Arora, Rishi |
| description | Aims The parasympathetic nervous system is thought to play a key role in atrial fibrillation (AF). Since parasympathetic signalling is primarily mediated by the heterotrimeric G-protein, Gαiβγ, we hypothesized that targeted inhibition of Gαi interactions in the posterior left atrium (PLA) would modify the substrate for vagal AF. Methods and results Cell-penetrating(cp)-Gαi1/2 and cp-Gαi3 C-terminal peptides were assessed for their ability to attenuate cholinergic-parasympathetic signalling in isolated feline atrial myocytes and in canine left atrium (LA). Confocal fluorescence microscopy indicated that cp-Gαi1/2 and/or cp-Gαi3 peptides moderated carbachol attenuation of cellular Ca2+ transients in isolated atrial myocytes. High-density epicardial mapping of dog PLA, left atrial pulmonary veins (PVs), and left atrial appendage (LAA) indicated that the delivery of cp-Gαi1/2 peptide or cp-Gαi3 peptide into the PLA prolonged effective refractory periods at baseline and during vagal stimulation in the PLA and to varying extents also in the LAA and PV regions. After delivery of cp-Gαi peptides into the PLA, AF inducibility during vagal stimulation was significantly diminished. Conclusion These results demonstrate the feasibility of using specific Gi-protein inhibition to achieve selective parasympathetic denervation in the PLA, with a resulting change in vagal responsiveness across the entire LA. |
| doi_str_mv | 10.1093/cvr/cvp148 |
| format | Article |
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Andrew ; Goldberger, Jeffrey J. ; Kadish, Alan H. ; Arora, Rishi</creator><creatorcontrib>Aistrup, Gary L. ; Villuendas, Roger ; Ng, Jason ; Gilchrist, Annette ; Lynch, Thomas W. ; Gordon, David ; Cokic, Ivan ; Mottl, Steven ; Zhou, Rui ; Dean, David A. ; Wasserstrom, J. Andrew ; Goldberger, Jeffrey J. ; Kadish, Alan H. ; Arora, Rishi</creatorcontrib><description>Aims The parasympathetic nervous system is thought to play a key role in atrial fibrillation (AF). Since parasympathetic signalling is primarily mediated by the heterotrimeric G-protein, Gαiβγ, we hypothesized that targeted inhibition of Gαi interactions in the posterior left atrium (PLA) would modify the substrate for vagal AF. Methods and results Cell-penetrating(cp)-Gαi1/2 and cp-Gαi3 C-terminal peptides were assessed for their ability to attenuate cholinergic-parasympathetic signalling in isolated feline atrial myocytes and in canine left atrium (LA). Confocal fluorescence microscopy indicated that cp-Gαi1/2 and/or cp-Gαi3 peptides moderated carbachol attenuation of cellular Ca2+ transients in isolated atrial myocytes. High-density epicardial mapping of dog PLA, left atrial pulmonary veins (PVs), and left atrial appendage (LAA) indicated that the delivery of cp-Gαi1/2 peptide or cp-Gαi3 peptide into the PLA prolonged effective refractory periods at baseline and during vagal stimulation in the PLA and to varying extents also in the LAA and PV regions. After delivery of cp-Gαi peptides into the PLA, AF inducibility during vagal stimulation was significantly diminished. Conclusion These results demonstrate the feasibility of using specific Gi-protein inhibition to achieve selective parasympathetic denervation in the PLA, with a resulting change in vagal responsiveness across the entire LA.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1093/cvr/cvp148</identifier><identifier>PMID: 19457892</identifier><identifier>CODEN: CVREAU</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Action Potentials ; Animals ; Atrial fibrillation ; Atrial Fibrillation - drug therapy ; Atrial Fibrillation - metabolism ; Atrial Fibrillation - physiopathology ; Atrial refractoriness ; Biological and medical sciences ; Calcium Signaling - drug effects ; Calcium transient ; Carbachol - pharmacology ; Cardiac dysrhythmias ; Cardiology. Vascular system ; Cardiovascular Agents - pharmacology ; Cats ; Cholinergic Agonists - pharmacology ; Cyclic AMP - metabolism ; Dogs ; E-C coupling ; G-proteins ; GTP-Binding Protein alpha Subunits, Gi-Go - antagonists & inhibitors ; GTP-Binding Protein alpha Subunits, Gi-Go - metabolism ; GTP-Binding Protein beta Subunits - metabolism ; GTP-Binding Protein gamma Subunits - metabolism ; Heart ; Heart Atria - drug effects ; Heart Atria - innervation ; Heart Atria - metabolism ; Medical sciences ; Microscopy, Confocal ; Muscarinic ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Original ; Parasympathectomy - methods ; Parasympathetic ; Peptides - pharmacology ; Potassium - metabolism ; Receptor, Muscarinic M2 - metabolism ; Refractory Period, Electrophysiological ; Signal transduction ; Time Factors ; Vagus Nerve - drug effects ; Vagus Nerve - metabolism ; Vagus Nerve - physiopathology</subject><ispartof>Cardiovascular research, 2009-08, Vol.83 (3), p.481-492</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org. 2009</rights><rights>2009 INIST-CNRS</rights><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-19ce539019833c6578bde0017900594a29cc5c6520962c6bd521b10bbe0000c43</citedby><cites>FETCH-LOGICAL-c540t-19ce539019833c6578bde0017900594a29cc5c6520962c6bd521b10bbe0000c43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,1584,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21698882$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19457892$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aistrup, Gary L.</creatorcontrib><creatorcontrib>Villuendas, Roger</creatorcontrib><creatorcontrib>Ng, Jason</creatorcontrib><creatorcontrib>Gilchrist, Annette</creatorcontrib><creatorcontrib>Lynch, Thomas W.</creatorcontrib><creatorcontrib>Gordon, David</creatorcontrib><creatorcontrib>Cokic, Ivan</creatorcontrib><creatorcontrib>Mottl, Steven</creatorcontrib><creatorcontrib>Zhou, Rui</creatorcontrib><creatorcontrib>Dean, David A.</creatorcontrib><creatorcontrib>Wasserstrom, J. Andrew</creatorcontrib><creatorcontrib>Goldberger, Jeffrey J.</creatorcontrib><creatorcontrib>Kadish, Alan H.</creatorcontrib><creatorcontrib>Arora, Rishi</creatorcontrib><title>Targeted G-protein inhibition as a novel approach to decrease vagal atrial fibrillation by selective parasympathetic attenuation</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>Aims The parasympathetic nervous system is thought to play a key role in atrial fibrillation (AF). Since parasympathetic signalling is primarily mediated by the heterotrimeric G-protein, Gαiβγ, we hypothesized that targeted inhibition of Gαi interactions in the posterior left atrium (PLA) would modify the substrate for vagal AF. Methods and results Cell-penetrating(cp)-Gαi1/2 and cp-Gαi3 C-terminal peptides were assessed for their ability to attenuate cholinergic-parasympathetic signalling in isolated feline atrial myocytes and in canine left atrium (LA). Confocal fluorescence microscopy indicated that cp-Gαi1/2 and/or cp-Gαi3 peptides moderated carbachol attenuation of cellular Ca2+ transients in isolated atrial myocytes. High-density epicardial mapping of dog PLA, left atrial pulmonary veins (PVs), and left atrial appendage (LAA) indicated that the delivery of cp-Gαi1/2 peptide or cp-Gαi3 peptide into the PLA prolonged effective refractory periods at baseline and during vagal stimulation in the PLA and to varying extents also in the LAA and PV regions. After delivery of cp-Gαi peptides into the PLA, AF inducibility during vagal stimulation was significantly diminished. Conclusion These results demonstrate the feasibility of using specific Gi-protein inhibition to achieve selective parasympathetic denervation in the PLA, with a resulting change in vagal responsiveness across the entire LA.</description><subject>Action Potentials</subject><subject>Animals</subject><subject>Atrial fibrillation</subject><subject>Atrial Fibrillation - drug therapy</subject><subject>Atrial Fibrillation - metabolism</subject><subject>Atrial Fibrillation - physiopathology</subject><subject>Atrial refractoriness</subject><subject>Biological and medical sciences</subject><subject>Calcium Signaling - drug effects</subject><subject>Calcium transient</subject><subject>Carbachol - pharmacology</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular Agents - pharmacology</subject><subject>Cats</subject><subject>Cholinergic Agonists - pharmacology</subject><subject>Cyclic AMP - metabolism</subject><subject>Dogs</subject><subject>E-C coupling</subject><subject>G-proteins</subject><subject>GTP-Binding Protein alpha Subunits, Gi-Go - antagonists & inhibitors</subject><subject>GTP-Binding Protein alpha Subunits, Gi-Go - metabolism</subject><subject>GTP-Binding Protein beta Subunits - metabolism</subject><subject>GTP-Binding Protein gamma Subunits - metabolism</subject><subject>Heart</subject><subject>Heart Atria - drug effects</subject><subject>Heart Atria - innervation</subject><subject>Heart Atria - metabolism</subject><subject>Medical sciences</subject><subject>Microscopy, Confocal</subject><subject>Muscarinic</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Original</subject><subject>Parasympathectomy - methods</subject><subject>Parasympathetic</subject><subject>Peptides - pharmacology</subject><subject>Potassium - metabolism</subject><subject>Receptor, Muscarinic M2 - metabolism</subject><subject>Refractory Period, Electrophysiological</subject><subject>Signal transduction</subject><subject>Time Factors</subject><subject>Vagus Nerve - drug effects</subject><subject>Vagus Nerve - metabolism</subject><subject>Vagus Nerve - physiopathology</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFr2zAUxkVZabN2l_0BQ5ddCl4ly7Kty2CUpRkEyiCDsot4kl8SbY5tJMUst_7pU5uQtpcexEP6fu97kj5CPnL2hTMlru3o0xp4UZ-QCa-kzEReyHdkwhirs1KU4py8D-FP2kpZFWfknKtCVrXKJ-RhAX6FERt6mw2-j-g66rq1My66vqMQKNCuH7GlMCQd7JrGnjZoPUJAOsIKkhS9S2XpjHdtC0-dZkcDtmijG5EO4CHsNgPENUZnU0PEbvsEXpLTJbQBPxzqBfk1_b64mWXzu9sfN9_mmZUFixlXFqVQjKtaCFum25sGGeOVSo9SBeTKWpnOc6bK3JamkTk3nBmTIMZsIS7I173vsDUbbCx20UOrB-824He6B6dfK51b61U_6rxiqigfDa72Btb3IXhcHns504856JSD3ueQ4E8vpz2jh49PwOcDAMFCu_TQWReOXM5LVdf1C67fDm8PzPacCxH_HUnwf3VZiUrq2f1vXU9_svlsutBT8R-B3rEF</recordid><startdate>20090801</startdate><enddate>20090801</enddate><creator>Aistrup, Gary L.</creator><creator>Villuendas, Roger</creator><creator>Ng, Jason</creator><creator>Gilchrist, Annette</creator><creator>Lynch, Thomas W.</creator><creator>Gordon, David</creator><creator>Cokic, Ivan</creator><creator>Mottl, Steven</creator><creator>Zhou, Rui</creator><creator>Dean, David A.</creator><creator>Wasserstrom, J. Andrew</creator><creator>Goldberger, Jeffrey J.</creator><creator>Kadish, Alan H.</creator><creator>Arora, Rishi</creator><general>Oxford University Press</general><scope>BSCLL</scope><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>5PM</scope></search><sort><creationdate>20090801</creationdate><title>Targeted G-protein inhibition as a novel approach to decrease vagal atrial fibrillation by selective parasympathetic attenuation</title><author>Aistrup, Gary L. ; Villuendas, Roger ; Ng, Jason ; Gilchrist, Annette ; Lynch, Thomas W. ; Gordon, David ; Cokic, Ivan ; Mottl, Steven ; Zhou, Rui ; Dean, David A. ; Wasserstrom, J. Andrew ; Goldberger, Jeffrey J. ; Kadish, Alan H. ; Arora, Rishi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-19ce539019833c6578bde0017900594a29cc5c6520962c6bd521b10bbe0000c43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Action Potentials</topic><topic>Animals</topic><topic>Atrial fibrillation</topic><topic>Atrial Fibrillation - drug therapy</topic><topic>Atrial Fibrillation - metabolism</topic><topic>Atrial Fibrillation - physiopathology</topic><topic>Atrial refractoriness</topic><topic>Biological and medical sciences</topic><topic>Calcium Signaling - drug effects</topic><topic>Calcium transient</topic><topic>Carbachol - pharmacology</topic><topic>Cardiac dysrhythmias</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular Agents - pharmacology</topic><topic>Cats</topic><topic>Cholinergic Agonists - pharmacology</topic><topic>Cyclic AMP - metabolism</topic><topic>Dogs</topic><topic>E-C coupling</topic><topic>G-proteins</topic><topic>GTP-Binding Protein alpha Subunits, Gi-Go - antagonists & inhibitors</topic><topic>GTP-Binding Protein alpha Subunits, Gi-Go - metabolism</topic><topic>GTP-Binding Protein beta Subunits - metabolism</topic><topic>GTP-Binding Protein gamma Subunits - metabolism</topic><topic>Heart</topic><topic>Heart Atria - drug effects</topic><topic>Heart Atria - innervation</topic><topic>Heart Atria - metabolism</topic><topic>Medical sciences</topic><topic>Microscopy, Confocal</topic><topic>Muscarinic</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Original</topic><topic>Parasympathectomy - methods</topic><topic>Parasympathetic</topic><topic>Peptides - pharmacology</topic><topic>Potassium - metabolism</topic><topic>Receptor, Muscarinic M2 - metabolism</topic><topic>Refractory Period, Electrophysiological</topic><topic>Signal transduction</topic><topic>Time Factors</topic><topic>Vagus Nerve - drug effects</topic><topic>Vagus Nerve - metabolism</topic><topic>Vagus Nerve - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aistrup, Gary L.</creatorcontrib><creatorcontrib>Villuendas, Roger</creatorcontrib><creatorcontrib>Ng, Jason</creatorcontrib><creatorcontrib>Gilchrist, Annette</creatorcontrib><creatorcontrib>Lynch, Thomas W.</creatorcontrib><creatorcontrib>Gordon, David</creatorcontrib><creatorcontrib>Cokic, Ivan</creatorcontrib><creatorcontrib>Mottl, Steven</creatorcontrib><creatorcontrib>Zhou, Rui</creatorcontrib><creatorcontrib>Dean, David A.</creatorcontrib><creatorcontrib>Wasserstrom, J. Andrew</creatorcontrib><creatorcontrib>Goldberger, Jeffrey J.</creatorcontrib><creatorcontrib>Kadish, Alan H.</creatorcontrib><creatorcontrib>Arora, Rishi</creatorcontrib><collection>Istex</collection><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>PubMed Central (Full Participant titles)</collection><jtitle>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aistrup, Gary L.</au><au>Villuendas, Roger</au><au>Ng, Jason</au><au>Gilchrist, Annette</au><au>Lynch, Thomas W.</au><au>Gordon, David</au><au>Cokic, Ivan</au><au>Mottl, Steven</au><au>Zhou, Rui</au><au>Dean, David A.</au><au>Wasserstrom, J. Andrew</au><au>Goldberger, Jeffrey J.</au><au>Kadish, Alan H.</au><au>Arora, Rishi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeted G-protein inhibition as a novel approach to decrease vagal atrial fibrillation by selective parasympathetic attenuation</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>2009-08-01</date><risdate>2009</risdate><volume>83</volume><issue>3</issue><spage>481</spage><epage>492</epage><pages>481-492</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><coden>CVREAU</coden><abstract>Aims The parasympathetic nervous system is thought to play a key role in atrial fibrillation (AF). Since parasympathetic signalling is primarily mediated by the heterotrimeric G-protein, Gαiβγ, we hypothesized that targeted inhibition of Gαi interactions in the posterior left atrium (PLA) would modify the substrate for vagal AF. Methods and results Cell-penetrating(cp)-Gαi1/2 and cp-Gαi3 C-terminal peptides were assessed for their ability to attenuate cholinergic-parasympathetic signalling in isolated feline atrial myocytes and in canine left atrium (LA). Confocal fluorescence microscopy indicated that cp-Gαi1/2 and/or cp-Gαi3 peptides moderated carbachol attenuation of cellular Ca2+ transients in isolated atrial myocytes. High-density epicardial mapping of dog PLA, left atrial pulmonary veins (PVs), and left atrial appendage (LAA) indicated that the delivery of cp-Gαi1/2 peptide or cp-Gαi3 peptide into the PLA prolonged effective refractory periods at baseline and during vagal stimulation in the PLA and to varying extents also in the LAA and PV regions. After delivery of cp-Gαi peptides into the PLA, AF inducibility during vagal stimulation was significantly diminished. Conclusion These results demonstrate the feasibility of using specific Gi-protein inhibition to achieve selective parasympathetic denervation in the PLA, with a resulting change in vagal responsiveness across the entire LA.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>19457892</pmid><doi>10.1093/cvr/cvp148</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | Action Potentials Animals Atrial fibrillation Atrial Fibrillation - drug therapy Atrial Fibrillation - metabolism Atrial Fibrillation - physiopathology Atrial refractoriness Biological and medical sciences Calcium Signaling - drug effects Calcium transient Carbachol - pharmacology Cardiac dysrhythmias Cardiology. Vascular system Cardiovascular Agents - pharmacology Cats Cholinergic Agonists - pharmacology Cyclic AMP - metabolism Dogs E-C coupling G-proteins GTP-Binding Protein alpha Subunits, Gi-Go - antagonists & inhibitors GTP-Binding Protein alpha Subunits, Gi-Go - metabolism GTP-Binding Protein beta Subunits - metabolism GTP-Binding Protein gamma Subunits - metabolism Heart Heart Atria - drug effects Heart Atria - innervation Heart Atria - metabolism Medical sciences Microscopy, Confocal Muscarinic Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Original Parasympathectomy - methods Parasympathetic Peptides - pharmacology Potassium - metabolism Receptor, Muscarinic M2 - metabolism Refractory Period, Electrophysiological Signal transduction Time Factors Vagus Nerve - drug effects Vagus Nerve - metabolism Vagus Nerve - physiopathology |
| title | Targeted G-protein inhibition as a novel approach to decrease vagal atrial fibrillation by selective parasympathetic attenuation |
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