Systems approach to the study of stretch and arrhythmias in right ventricular failure induced in rats by monocrotaline.
Identifieur interne : 003464 ( PubMed/Curation ); précédent : 003463; suivant : 003465Systems approach to the study of stretch and arrhythmias in right ventricular failure induced in rats by monocrotaline.
Auteurs : David Benoist [France] ; Rachel Stones [Royaume-Uni] ; Alan P. Benson [Royaume-Uni] ; Ewan D. Fowler [Royaume-Uni] ; Mark J. Drinkhill [Royaume-Uni] ; Matthew E L. Hardy [Royaume-Uni] ; David A. Saint [Australie] ; Olivier Cazorla [France] ; Olivier Bernus [France] ; Ed White [Royaume-Uni]Source :
- Progress in biophysics and molecular biology [ 1873-1732 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Biologie des systèmes (), Canaux ioniques (métabolisme), Contrainte mécanique, Couplage excitation-contraction, Dysfonction ventriculaire droite (), Dysfonction ventriculaire droite (physiopathologie), Hypertension pulmonaire (), Hypertension pulmonaire (physiopathologie), Module d'élasticité, Monocrotaline, Mécanotransduction cellulaire, Ouverture et fermeture des portes des canaux ioniques, Rat Wistar, Rats, Remodelage ventriculaire, Stimulation physique (), Système de conduction du coeur (), Système de conduction du coeur (physiopathologie), Troubles du rythme cardiaque (), Troubles du rythme cardiaque (physiopathologie).
- MESH :
- métabolisme : Canaux ioniques.
- physiopathologie : Dysfonction ventriculaire droite, Hypertension pulmonaire, Système de conduction du coeur, Troubles du rythme cardiaque.
- Animaux, Biologie des systèmes, Contrainte mécanique, Couplage excitation-contraction, Dysfonction ventriculaire droite, Hypertension pulmonaire, Module d'élasticité, Monocrotaline, Mécanotransduction cellulaire, Ouverture et fermeture des portes des canaux ioniques, Rat Wistar, Rats, Remodelage ventriculaire, Stimulation physique, Système de conduction du coeur, Troubles du rythme cardiaque.
English descriptors
- KwdEn :
- Animals, Arrhythmias, Cardiac (chemically induced), Arrhythmias, Cardiac (physiopathology), Elastic Modulus, Excitation Contraction Coupling, Heart Conduction System (drug effects), Heart Conduction System (physiopathology), Hypertension, Pulmonary (chemically induced), Hypertension, Pulmonary (physiopathology), Ion Channel Gating, Ion Channels (metabolism), Mechanotransduction, Cellular, Monocrotaline, Physical Stimulation (methods), Rats, Rats, Wistar, Stress, Mechanical, Systems Biology (methods), Ventricular Dysfunction, Right (chemically induced), Ventricular Dysfunction, Right (physiopathology), Ventricular Remodeling.
- MESH :
- chemical , metabolism : Ion Channels.
- chemically induced : Arrhythmias, Cardiac, Hypertension, Pulmonary, Ventricular Dysfunction, Right.
- drug effects : Heart Conduction System.
- methods : Physical Stimulation, Systems Biology.
- physiopathology : Arrhythmias, Cardiac, Heart Conduction System, Hypertension, Pulmonary, Ventricular Dysfunction, Right.
- Animals, Elastic Modulus, Excitation Contraction Coupling, Ion Channel Gating, Mechanotransduction, Cellular, Monocrotaline, Rats, Rats, Wistar, Stress, Mechanical, Ventricular Remodeling.
Abstract
We demonstrate the synergistic benefits of using multiple technologies to investigate complex multi-scale biological responses. The combination of reductionist and integrative methodologies can reveal novel insights into mechanisms of action by tracking changes of in vivo phenomena to alterations in protein activity (or vice versa). We have applied this approach to electrical and mechanical remodelling in right ventricular failure caused by monocrotaline-induced pulmonary artery hypertension in rats. We show arrhythmogenic T-wave alternans in the ECG of conscious heart failure animals. Optical mapping of isolated hearts revealed discordant action potential duration (APD) alternans. Potential causes of the arrhythmic substrate; structural remodelling and/or steep APD restitution and dispersion were observed, with specific remodelling of the Right Ventricular Outflow Tract. At the myocyte level, [Ca(2+)]i transient alternans were observed together with decreased activity, gene and protein expression of the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA). Computer simulations of the electrical and structural remodelling suggest both contribute to a less stable substrate. Echocardiography was used to estimate increased wall stress in failure, in vivo. Stretch of intact and skinned single myocytes revealed no effect on the Frank-Starling mechanism in failing myocytes. In isolated hearts acute stretch-induced arrhythmias occurred in all preparations. Significant shortening of the early APD was seen in control but not failing hearts. These observations may be linked to changes in the gene expression of candidate mechanosensitive ion channels (MSCs) TREK-1 and TRPC1/6. Computer simulations incorporating MSCs and changes in ion channels with failure, based on altered gene expression, largely reproduced experimental observations.
DOI: 10.1016/j.pbiomolbio.2014.06.008
PubMed: 25016242
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Electronic address: e.white@leeds.ac.uk.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Multidisciplinary Cardiovascular Research Centre, University of Leeds</wicri:regionArea></affiliation></author></analytic><series><title level="j">Progress in biophysics and molecular biology</title><idno type="eISSN">1873-1732</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Arrhythmias, Cardiac (chemically induced)</term><term>Arrhythmias, Cardiac (physiopathology)</term><term>Elastic Modulus</term><term>Excitation Contraction Coupling</term><term>Heart Conduction System (drug effects)</term><term>Heart Conduction System (physiopathology)</term><term>Hypertension, Pulmonary (chemically induced)</term><term>Hypertension, Pulmonary (physiopathology)</term><term>Ion Channel Gating</term><term>Ion Channels (metabolism)</term><term>Mechanotransduction, Cellular</term><term>Monocrotaline</term><term>Physical Stimulation (methods)</term><term>Rats</term><term>Rats, Wistar</term><term>Stress, Mechanical</term><term>Systems Biology (methods)</term><term>Ventricular Dysfunction, Right (chemically induced)</term><term>Ventricular Dysfunction, Right (physiopathology)</term><term>Ventricular Remodeling</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Biologie des systèmes ()</term><term>Canaux ioniques (métabolisme)</term><term>Contrainte mécanique</term><term>Couplage excitation-contraction</term><term>Dysfonction ventriculaire droite ()</term><term>Dysfonction ventriculaire droite (physiopathologie)</term><term>Hypertension pulmonaire ()</term><term>Hypertension pulmonaire (physiopathologie)</term><term>Module d'élasticité</term><term>Monocrotaline</term><term>Mécanotransduction cellulaire</term><term>Ouverture et fermeture des portes des canaux ioniques</term><term>Rat Wistar</term><term>Rats</term><term>Remodelage ventriculaire</term><term>Stimulation physique ()</term><term>Système de conduction du coeur ()</term><term>Système de conduction du coeur (physiopathologie)</term><term>Troubles du rythme cardiaque ()</term><term>Troubles du rythme cardiaque (physiopathologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Ion Channels</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Arrhythmias, Cardiac</term><term>Hypertension, Pulmonary</term><term>Ventricular Dysfunction, Right</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Heart Conduction System</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Physical Stimulation</term><term>Systems Biology</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Canaux ioniques</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Dysfonction ventriculaire droite</term><term>Hypertension pulmonaire</term><term>Système de conduction du coeur</term><term>Troubles du rythme cardiaque</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Arrhythmias, Cardiac</term><term>Heart Conduction System</term><term>Hypertension, Pulmonary</term><term>Ventricular Dysfunction, Right</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Elastic Modulus</term><term>Excitation Contraction Coupling</term><term>Ion Channel Gating</term><term>Mechanotransduction, Cellular</term><term>Monocrotaline</term><term>Rats</term><term>Rats, Wistar</term><term>Stress, Mechanical</term><term>Ventricular Remodeling</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Biologie des systèmes</term><term>Contrainte mécanique</term><term>Couplage excitation-contraction</term><term>Dysfonction ventriculaire droite</term><term>Hypertension pulmonaire</term><term>Module d'élasticité</term><term>Monocrotaline</term><term>Mécanotransduction cellulaire</term><term>Ouverture et fermeture des portes des canaux ioniques</term><term>Rat Wistar</term><term>Rats</term><term>Remodelage ventriculaire</term><term>Stimulation physique</term><term>Système de conduction du coeur</term><term>Troubles du rythme cardiaque</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We demonstrate the synergistic benefits of using multiple technologies to investigate complex multi-scale biological responses. The combination of reductionist and integrative methodologies can reveal novel insights into mechanisms of action by tracking changes of in vivo phenomena to alterations in protein activity (or vice versa). We have applied this approach to electrical and mechanical remodelling in right ventricular failure caused by monocrotaline-induced pulmonary artery hypertension in rats. We show arrhythmogenic T-wave alternans in the ECG of conscious heart failure animals. Optical mapping of isolated hearts revealed discordant action potential duration (APD) alternans. Potential causes of the arrhythmic substrate; structural remodelling and/or steep APD restitution and dispersion were observed, with specific remodelling of the Right Ventricular Outflow Tract. At the myocyte level, [Ca(2+)]i transient alternans were observed together with decreased activity, gene and protein expression of the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA). Computer simulations of the electrical and structural remodelling suggest both contribute to a less stable substrate. Echocardiography was used to estimate increased wall stress in failure, in vivo. Stretch of intact and skinned single myocytes revealed no effect on the Frank-Starling mechanism in failing myocytes. In isolated hearts acute stretch-induced arrhythmias occurred in all preparations. Significant shortening of the early APD was seen in control but not failing hearts. These observations may be linked to changes in the gene expression of candidate mechanosensitive ion channels (MSCs) TREK-1 and TRPC1/6. Computer simulations incorporating MSCs and changes in ion channels with failure, based on altered gene expression, largely reproduced experimental observations.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25016242</PMID><DateCreated><Year>2014</Year><Month>12</Month><Day>02</Day></DateCreated><DateCompleted><Year>2015</Year><Month>08</Month><Day>24</Day></DateCompleted><DateRevised><Year>2017</Year><Month>09</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-1732</ISSN><JournalIssue CitedMedium="Internet"><Volume>115</Volume><Issue>2-3</Issue><PubDate><Year>2014</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Progress in biophysics and molecular biology</Title><ISOAbbreviation>Prog. Biophys. Mol. Biol.</ISOAbbreviation></Journal><ArticleTitle>Systems approach to the study of stretch and arrhythmias in right ventricular failure induced in rats by monocrotaline.</ArticleTitle><Pagination><MedlinePgn>162-72</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.pbiomolbio.2014.06.008</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0079-6107(14)00050-9</ELocationID><Abstract><AbstractText>We demonstrate the synergistic benefits of using multiple technologies to investigate complex multi-scale biological responses. The combination of reductionist and integrative methodologies can reveal novel insights into mechanisms of action by tracking changes of in vivo phenomena to alterations in protein activity (or vice versa). We have applied this approach to electrical and mechanical remodelling in right ventricular failure caused by monocrotaline-induced pulmonary artery hypertension in rats. We show arrhythmogenic T-wave alternans in the ECG of conscious heart failure animals. Optical mapping of isolated hearts revealed discordant action potential duration (APD) alternans. Potential causes of the arrhythmic substrate; structural remodelling and/or steep APD restitution and dispersion were observed, with specific remodelling of the Right Ventricular Outflow Tract. At the myocyte level, [Ca(2+)]i transient alternans were observed together with decreased activity, gene and protein expression of the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA). Computer simulations of the electrical and structural remodelling suggest both contribute to a less stable substrate. Echocardiography was used to estimate increased wall stress in failure, in vivo. Stretch of intact and skinned single myocytes revealed no effect on the Frank-Starling mechanism in failing myocytes. In isolated hearts acute stretch-induced arrhythmias occurred in all preparations. Significant shortening of the early APD was seen in control but not failing hearts. These observations may be linked to changes in the gene expression of candidate mechanosensitive ion channels (MSCs) TREK-1 and TRPC1/6. Computer simulations incorporating MSCs and changes in ion channels with failure, based on altered gene expression, largely reproduced experimental observations.</AbstractText><CopyrightInformation>Copyright © 2014 The Authors. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Benoist</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Multidisciplinary Cardiovascular Research Centre, University of Leeds, UK; L'Institut de Rythmologie et Modelisation Cardiaque, INSERM U1045, Université de Bordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stones</LastName><ForeName>Rachel</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Multidisciplinary Cardiovascular Research Centre, University of Leeds, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Benson</LastName><ForeName>Alan P</ForeName><Initials>AP</Initials><AffiliationInfo><Affiliation>Multidisciplinary Cardiovascular Research Centre, University of Leeds, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fowler</LastName><ForeName>Ewan D</ForeName><Initials>ED</Initials><AffiliationInfo><Affiliation>Multidisciplinary Cardiovascular Research Centre, University of Leeds, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Drinkhill</LastName><ForeName>Mark J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Multidisciplinary Cardiovascular Research Centre, University of Leeds, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hardy</LastName><ForeName>Matthew E L</ForeName><Initials>ME</Initials><AffiliationInfo><Affiliation>Multidisciplinary Cardiovascular Research Centre, University of Leeds, UK; Faculty of Life Sciences, University of Manchester, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saint</LastName><ForeName>David A</ForeName><Initials>DA</Initials><AffiliationInfo><Affiliation>School of Medical Sciences, University of Adelaide, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cazorla</LastName><ForeName>Olivier</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>INSERM U1046, Université Montpellier 1, Université Montpellier 2, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bernus</LastName><ForeName>Olivier</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Multidisciplinary Cardiovascular Research Centre, University of Leeds, UK; L'Institut de Rythmologie et Modelisation Cardiaque, INSERM U1045, Université de Bordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>White</LastName><ForeName>Ed</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Multidisciplinary Cardiovascular Research Centre, University of Leeds, UK. Electronic address: e.white@leeds.ac.uk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>G0900524</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>PG/08/027/24774</GrantID><Agency>British Heart Foundation</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>British Heart Foundation</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>07</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Prog Biophys Mol Biol</MedlineTA><NlmUniqueID>0401233</NlmUniqueID><ISSNLinking>0079-6107</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007473">Ion Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>73077K8HYV</RegistryNumber><NameOfSubstance UI="D016686">Monocrotaline</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Mol Cell Cardiol. 2013 Mar;56:91-6</RefSource><PMID Version="1">23261965</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circulation. 1992 Sep;86(3):968-78</RefSource><PMID Version="1">1381296</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Physiol. 2004 Aug 15;559(Pt 1):205-14</RefSource><PMID Version="1">15235080</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Heart Circ Physiol. 2002 Jul;283(1):H364-71</RefSource><PMID Version="1">12063310</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Heart Circ Physiol. 2011 Jun;300(6):H2230-7</RefSource><PMID Version="1">21398591</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2007 Jun 8;100(11):1605-14</RefSource><PMID Version="1">17478725</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Pharm Des. 2006;12(28):3645-63</RefSource><PMID Version="1">17073665</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur Heart J. 2009 Oct;30(20):2493-537</RefSource><PMID Version="1">19713419</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Heart Circ Physiol. 2012 Jun 1;302(11):H2381-95</RefSource><PMID Version="1">22427523</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cardiovasc Res. 2006 Jan;69(1):86-97</RefSource><PMID Version="1">16248991</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Clin Pharmacol Ther. 2010 Jul;88(1):25-33</RefSource><PMID Version="1">20531468</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2005 Jan;19(1):88-90</RefSource><PMID Version="1">15498894</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Physiol. 2005 Jan 15;562(Pt 2):367-80</RefSource><PMID Version="1">15528244</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Pharmacol Ther. 2009 Jan;121(1):69-88</RefSource><PMID Version="1">19010350</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Hum Reprod. 2007 Mar;13(3):171-9</RefSource><PMID Version="1">17208928</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2011 Jan 7;108(1):98-112</RefSource><PMID Version="1">21212392</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Thorax. 1967 Mar;22(2):176-9</RefSource><PMID Version="1">6033385</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Naunyn Schmiedebergs Arch Pharmacol. 2006 Sep;373(6):391-400</RefSource><PMID Version="1">16932922</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Am Coll Cardiol. 2011 Feb 8;57(6):740-50</RefSource><PMID Version="1">21292134</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann N Y Acad Sci. 2005 Jun;1047:314-23</RefSource><PMID Version="1">16093507</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Pflugers Arch. 2008 Mar;455(6):1097-103</RefSource><PMID Version="1">17957383</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Huazhong Univ Sci Technolog Med Sci. 2007 Aug;27(4):385-7</RefSource><PMID Version="1">17828492</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cardiovasc Res. 1995 Apr;29(4):555-62</RefSource><PMID Version="1">7796450</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Heart Fail. 2012 Jan;5(1):97-105</RefSource><PMID Version="1">22157723</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Am Soc Echocardiogr. 2006 Oct;19(10):1272-9</RefSource><PMID Version="1">17000367</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Biophys Mol Biol. 2008 Jun-Jul;97(2-3):332-47</RefSource><PMID Version="1">18395246</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Huazhong Univ Sci Technolog Med Sci. 2006;26(1):31-3</RefSource><PMID Version="1">16711001</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Heart Fail. 2009 Jan;2(1):47-55</RefSource><PMID Version="1">19808315</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Physiol. 2011 Mar 1;589(Pt 5):1031-6</RefSource><PMID Version="1">21224223</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biophys J. 2001 Dec;81(6):3029-51</RefSource><PMID Version="1">11720973</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2004 Apr 30;94(8):1083-90</RefSource><PMID Version="1">15016735</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2001 Jan 4;409(6816):35-6</RefSource><PMID Version="1">11343101</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Pharmacol Rev. 1996 Jun;48(2):231-52</RefSource><PMID Version="1">8804105</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Pharmacol Ther. 2006 Dec;112(3):744-60</RefSource><PMID Version="1">16842858</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Calcium. 2009 Jan;45(1):38-54</RefSource><PMID Version="1">18635261</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Biophys Mol Biol. 2014 Aug;115(2-3):235-43</RefSource><PMID Version="1">25009995</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Biophys Mol Biol. 2012 Oct-Nov;110(2-3):331-9</RefSource><PMID Version="1">22824411</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur Respir Rev. 2010 Mar;19(115):4-6</RefSource><PMID Version="1">20956160</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Physiol Rev. 2001 Apr;81(2):685-740</RefSource><PMID Version="1">11274342</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Intensive Care Med. 2004 Feb;30(2):185-96</RefSource><PMID Version="1">14618229</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Pflugers Arch. 2005 Oct;451(1):53-60</RefSource><PMID Version="1">15965706</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circulation. 1994 Oct;90(4):2022-31</RefSource><PMID Version="1">7522991</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circulation. 2008 Apr 1;117(13):1717-31</RefSource><PMID Version="1">18378625</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Interface Focus. 2011 Feb 6;1(1):101-16</RefSource><PMID Version="1">22419977</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Mol Cell Cardiol. 2007 Mar;42(3):498-507</RefSource><PMID Version="1">17174323</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Europace. 2005 Sep;7 Suppl 2:128-34</RefSource><PMID Version="1">16102510</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Int J Cardiol. 2013 Aug 10;167(3):669-76</RefSource><PMID Version="1">22459397</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cardiovasc Res. 2000 Dec;48(3):409-20</RefSource><PMID Version="1">11090836</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Cell Biol. 2005 Feb;7(2):179-85</RefSource><PMID Version="1">15665854</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Basic Res Cardiol. 2009 Nov;104(6):643-52</RefSource><PMID Version="1">19415411</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Chest. 2009 Mar;135(3):794-804</RefSource><PMID Version="1">19265089</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Clin Exp Pharmacol Physiol. 2006 Jul;33(7):642-8</RefSource><PMID Version="1">16789934</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Chest. 1998 Jul;114(1 Suppl):101S-106S</RefSource><PMID Version="1">9676654</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Heart Rhythm. 2009 Mar;6(3 Suppl):S22-8</RefSource><PMID Version="1">19168395</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Electrocardiol. 2005 Oct;38(4 Suppl):154-8</RefSource><PMID Version="1">16226092</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Cell Biol. 2005 Feb;7(2):105-7</RefSource><PMID Version="1">15689975</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cardiovasc Res. 1997 Jun;34(3):493-503</RefSource><PMID Version="1">9231032</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Respir Crit Care Med. 2010 Sep 1;182(5):652-60</RefSource><PMID Version="1">20508210</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Physiol. 2011 Mar 1;589(Pt 5):1037-45</RefSource><PMID Version="1">21224228</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Front Physiol. 2010 Nov 29;1:154</RefSource><PMID Version="1">21286254</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circulation. 2006 Oct 24;114(17):1883-91</RefSource><PMID Version="1">17060398</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Biophys Mol Biol. 2014 Aug;115(2-3):186-97</RefSource><PMID Version="1">25077410</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Arrhythm Electrophysiol. 2010 Apr;3(2):195-203</RefSource><PMID Version="1">20133934</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055119" MajorTopicYN="N">Elastic Modulus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056966" MajorTopicYN="Y">Excitation Contraction Coupling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006329" MajorTopicYN="N">Heart Conduction System</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006976" MajorTopicYN="N">Hypertension, Pulmonary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015640" MajorTopicYN="N">Ion Channel Gating</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007473" MajorTopicYN="N">Ion Channels</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D040542" MajorTopicYN="Y">Mechanotransduction, Cellular</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016686" MajorTopicYN="N">Monocrotaline</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010812" MajorTopicYN="N">Physical Stimulation</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013314" MajorTopicYN="N">Stress, Mechanical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049490" MajorTopicYN="N">Systems Biology</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018497" MajorTopicYN="N">Ventricular Dysfunction, Right</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020257" MajorTopicYN="N">Ventricular Remodeling</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4210667</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Arrhythmias</Keyword><Keyword MajorTopicYN="N">Mechanosensitivity</Keyword><Keyword MajorTopicYN="N">Monocrotaline</Keyword><Keyword MajorTopicYN="N">Pulmonary artery hypertension</Keyword><Keyword MajorTopicYN="N">Systems Biology</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>06</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>06</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>7</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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