Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts

Autores
Durkina, Aleksandra V.; Szeiffova Bacova, Barbara; Bernikova, Olesya G.; Gonotkov, Mikhail A.; Sedova, Ksenia A.; Cuprova, Julie; Vaykshnorayte, Marina A.; Diez, Emiliano Raúl; Prado, Natalia Jorgelina; Azarov, Jan E.
Año de publicación
2023
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Melatonin has been reported to cause myocardial electrophysiological changes and prevent ventricular tachycardia or fibrillation (VT/VF) in ischemia and reperfusion. We sought to identify electrophysiological targets responsible for the melatonin antiarrhythmic action and to explore whether melatonin receptor-dependent pathways or its antioxidative properties are essential for these effects. Ischemia was induced in anesthetized rats given a placebo, melatonin, and/or luzindole (MT1/MT2 melatonin receptor blocker), and epicardial mapping with reperfusion VT/VFs assessment was performed. The oxidative stress assessment and Western blotting analysis were performed in the explanted hearts. Transmembrane potentials and ionic currents were recorded in cardiomyocytes with melatonin and/or luzindole application. Melatonin reduced reperfusion VT/VF incidence associated with local activation time in logistic regression analysis. Melatonin prevented ischemia-related conduction slowing and did not change the total connexin43 (Cx43) level or oxidative stress markers, but it increased the content of a phosphorylated Cx43 variant (P-Cx43368). Luzindole abolished the melatonin antiarrhythmic effect, slowed conduction, decreased total Cx43, protein kinase Cε and P-Cx43368 levels, and the IK1 current, and caused resting membrane potential (RMP) depolarization. Neither melatonin nor luzindole modified INa current. Thus, the antiarrhythmic effect of melatonin was mediated by the receptor-dependent enhancement of impulse conduction, which was associated with Cx43 phosphorylation and maintaining the RMP level.
Fil: Durkina, Aleksandra V.. Russian Academy Of Sciences. Center Of The Ural Branch. Institute Of Physiology Of The Komi Scientific; Rusia
Fil: Szeiffova Bacova, Barbara. Slovak Academy Of Sciences. Institute For Heart Research; Eslovaquia
Fil: Bernikova, Olesya G.. Russian Academy Of Sciences. Center Of The Ural Branch. Institute Of Physiology Of The Komi Scientific; Rusia
Fil: Gonotkov, Mikhail A.. Russian Academy Of Sciences. Center Of The Ural Branch. Institute Of Physiology Of The Komi Scientific; Rusia
Fil: Sedova, Ksenia A.. Czech Technical University; República Checa
Fil: Cuprova, Julie. Czech Technical University; República Checa
Fil: Vaykshnorayte, Marina A.. Russian Academy Of Sciences. Komi Scientific Center Of The Ural Branch. Institute Of Physiology ; Rusia
Fil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Azarov, Jan E.. Czech Technical University; República Checa. Russian Academy Of Sciences. The Komi Scientific Center Of The Ural Branch. Institute Of Physiology; Rusia
Materia
CONDUCTION VELOCITY
CONNEXIN-43
MELATONIN
POST-ISCHEMIC ARRHYTHMIAS
POTASSIUM CURRENT
RAT HEART
SODIUM CURRENT
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/248610
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/248610
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat heartsDurkina, Aleksandra V.Szeiffova Bacova, BarbaraBernikova, Olesya G.Gonotkov, Mikhail A.Sedova, Ksenia A.Cuprova, JulieVaykshnorayte, Marina A.Diez, Emiliano RaúlPrado, Natalia JorgelinaAzarov, Jan E.CONDUCTION VELOCITYCONNEXIN-43MELATONINPOST-ISCHEMIC ARRHYTHMIASPOTASSIUM CURRENTRAT HEARTSODIUM CURRENThttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Melatonin has been reported to cause myocardial electrophysiological changes and prevent ventricular tachycardia or fibrillation (VT/VF) in ischemia and reperfusion. We sought to identify electrophysiological targets responsible for the melatonin antiarrhythmic action and to explore whether melatonin receptor-dependent pathways or its antioxidative properties are essential for these effects. Ischemia was induced in anesthetized rats given a placebo, melatonin, and/or luzindole (MT1/MT2 melatonin receptor blocker), and epicardial mapping with reperfusion VT/VFs assessment was performed. The oxidative stress assessment and Western blotting analysis were performed in the explanted hearts. Transmembrane potentials and ionic currents were recorded in cardiomyocytes with melatonin and/or luzindole application. Melatonin reduced reperfusion VT/VF incidence associated with local activation time in logistic regression analysis. Melatonin prevented ischemia-related conduction slowing and did not change the total connexin43 (Cx43) level or oxidative stress markers, but it increased the content of a phosphorylated Cx43 variant (P-Cx43368). Luzindole abolished the melatonin antiarrhythmic effect, slowed conduction, decreased total Cx43, protein kinase Cε and P-Cx43368 levels, and the IK1 current, and caused resting membrane potential (RMP) depolarization. Neither melatonin nor luzindole modified INa current. Thus, the antiarrhythmic effect of melatonin was mediated by the receptor-dependent enhancement of impulse conduction, which was associated with Cx43 phosphorylation and maintaining the RMP level.Fil: Durkina, Aleksandra V.. Russian Academy Of Sciences. Center Of The Ural Branch. Institute Of Physiology Of The Komi Scientific; RusiaFil: Szeiffova Bacova, Barbara. Slovak Academy Of Sciences. Institute For Heart Research; EslovaquiaFil: Bernikova, Olesya G.. Russian Academy Of Sciences. Center Of The Ural Branch. Institute Of Physiology Of The Komi Scientific; RusiaFil: Gonotkov, Mikhail A.. Russian Academy Of Sciences. Center Of The Ural Branch. Institute Of Physiology Of The Komi Scientific; RusiaFil: Sedova, Ksenia A.. Czech Technical University; República ChecaFil: Cuprova, Julie. Czech Technical University; República ChecaFil: Vaykshnorayte, Marina A.. Russian Academy Of Sciences. Komi Scientific Center Of The Ural Branch. Institute Of Physiology ; RusiaFil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Azarov, Jan E.. Czech Technical University; República Checa. Russian Academy Of Sciences. The Komi Scientific Center Of The Ural Branch. Institute Of Physiology; RusiaMolecular Diversity Preservation International2023-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/248610Durkina, Aleksandra V.; Szeiffova Bacova, Barbara; Bernikova, Olesya G.; Gonotkov, Mikhail A.; Sedova, Ksenia A.; et al.; Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts; Molecular Diversity Preservation International; International Journal of Molecular Sciences; 24; 15; 8-2023; 1-161661-65961422-0067CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/1422-0067/24/15/11931info:eu-repo/semantics/altIdentifier/doi/10.3390/ijms241511931info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:48:42Zoai:ri.conicet.gov.ar:11336/248610instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:48:42.96CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts
title Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts
spellingShingle Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts
Durkina, Aleksandra V.
CONDUCTION VELOCITY
CONNEXIN-43
MELATONIN
POST-ISCHEMIC ARRHYTHMIAS
POTASSIUM CURRENT
RAT HEART
SODIUM CURRENT
title_short Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts
title_full Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts
title_fullStr Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts
title_full_unstemmed Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts
title_sort Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts
dc.creator.none.fl_str_mv Durkina, Aleksandra V.
Szeiffova Bacova, Barbara
Bernikova, Olesya G.
Gonotkov, Mikhail A.
Sedova, Ksenia A.
Cuprova, Julie
Vaykshnorayte, Marina A.
Diez, Emiliano Raúl
Prado, Natalia Jorgelina
Azarov, Jan E.
author Durkina, Aleksandra V.
author_facet Durkina, Aleksandra V.
Szeiffova Bacova, Barbara
Bernikova, Olesya G.
Gonotkov, Mikhail A.
Sedova, Ksenia A.
Cuprova, Julie
Vaykshnorayte, Marina A.
Diez, Emiliano Raúl
Prado, Natalia Jorgelina
Azarov, Jan E.
author_role author
author2 Szeiffova Bacova, Barbara
Bernikova, Olesya G.
Gonotkov, Mikhail A.
Sedova, Ksenia A.
Cuprova, Julie
Vaykshnorayte, Marina A.
Diez, Emiliano Raúl
Prado, Natalia Jorgelina
Azarov, Jan E.
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv CONDUCTION VELOCITY
CONNEXIN-43
MELATONIN
POST-ISCHEMIC ARRHYTHMIAS
POTASSIUM CURRENT
RAT HEART
SODIUM CURRENT
topic CONDUCTION VELOCITY
CONNEXIN-43
MELATONIN
POST-ISCHEMIC ARRHYTHMIAS
POTASSIUM CURRENT
RAT HEART
SODIUM CURRENT
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Melatonin has been reported to cause myocardial electrophysiological changes and prevent ventricular tachycardia or fibrillation (VT/VF) in ischemia and reperfusion. We sought to identify electrophysiological targets responsible for the melatonin antiarrhythmic action and to explore whether melatonin receptor-dependent pathways or its antioxidative properties are essential for these effects. Ischemia was induced in anesthetized rats given a placebo, melatonin, and/or luzindole (MT1/MT2 melatonin receptor blocker), and epicardial mapping with reperfusion VT/VFs assessment was performed. The oxidative stress assessment and Western blotting analysis were performed in the explanted hearts. Transmembrane potentials and ionic currents were recorded in cardiomyocytes with melatonin and/or luzindole application. Melatonin reduced reperfusion VT/VF incidence associated with local activation time in logistic regression analysis. Melatonin prevented ischemia-related conduction slowing and did not change the total connexin43 (Cx43) level or oxidative stress markers, but it increased the content of a phosphorylated Cx43 variant (P-Cx43368). Luzindole abolished the melatonin antiarrhythmic effect, slowed conduction, decreased total Cx43, protein kinase Cε and P-Cx43368 levels, and the IK1 current, and caused resting membrane potential (RMP) depolarization. Neither melatonin nor luzindole modified INa current. Thus, the antiarrhythmic effect of melatonin was mediated by the receptor-dependent enhancement of impulse conduction, which was associated with Cx43 phosphorylation and maintaining the RMP level.
Fil: Durkina, Aleksandra V.. Russian Academy Of Sciences. Center Of The Ural Branch. Institute Of Physiology Of The Komi Scientific; Rusia
Fil: Szeiffova Bacova, Barbara. Slovak Academy Of Sciences. Institute For Heart Research; Eslovaquia
Fil: Bernikova, Olesya G.. Russian Academy Of Sciences. Center Of The Ural Branch. Institute Of Physiology Of The Komi Scientific; Rusia
Fil: Gonotkov, Mikhail A.. Russian Academy Of Sciences. Center Of The Ural Branch. Institute Of Physiology Of The Komi Scientific; Rusia
Fil: Sedova, Ksenia A.. Czech Technical University; República Checa
Fil: Cuprova, Julie. Czech Technical University; República Checa
Fil: Vaykshnorayte, Marina A.. Russian Academy Of Sciences. Komi Scientific Center Of The Ural Branch. Institute Of Physiology ; Rusia
Fil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Azarov, Jan E.. Czech Technical University; República Checa. Russian Academy Of Sciences. The Komi Scientific Center Of The Ural Branch. Institute Of Physiology; Rusia
description Melatonin has been reported to cause myocardial electrophysiological changes and prevent ventricular tachycardia or fibrillation (VT/VF) in ischemia and reperfusion. We sought to identify electrophysiological targets responsible for the melatonin antiarrhythmic action and to explore whether melatonin receptor-dependent pathways or its antioxidative properties are essential for these effects. Ischemia was induced in anesthetized rats given a placebo, melatonin, and/or luzindole (MT1/MT2 melatonin receptor blocker), and epicardial mapping with reperfusion VT/VFs assessment was performed. The oxidative stress assessment and Western blotting analysis were performed in the explanted hearts. Transmembrane potentials and ionic currents were recorded in cardiomyocytes with melatonin and/or luzindole application. Melatonin reduced reperfusion VT/VF incidence associated with local activation time in logistic regression analysis. Melatonin prevented ischemia-related conduction slowing and did not change the total connexin43 (Cx43) level or oxidative stress markers, but it increased the content of a phosphorylated Cx43 variant (P-Cx43368). Luzindole abolished the melatonin antiarrhythmic effect, slowed conduction, decreased total Cx43, protein kinase Cε and P-Cx43368 levels, and the IK1 current, and caused resting membrane potential (RMP) depolarization. Neither melatonin nor luzindole modified INa current. Thus, the antiarrhythmic effect of melatonin was mediated by the receptor-dependent enhancement of impulse conduction, which was associated with Cx43 phosphorylation and maintaining the RMP level.
publishDate 2023
dc.date.none.fl_str_mv 2023-08
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/248610
Durkina, Aleksandra V.; Szeiffova Bacova, Barbara; Bernikova, Olesya G.; Gonotkov, Mikhail A.; Sedova, Ksenia A.; et al.; Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts; Molecular Diversity Preservation International; International Journal of Molecular Sciences; 24; 15; 8-2023; 1-16
1661-6596
1422-0067
CONICET Digital
CONICET
url http://hdl.handle.net/11336/248610
identifier_str_mv Durkina, Aleksandra V.; Szeiffova Bacova, Barbara; Bernikova, Olesya G.; Gonotkov, Mikhail A.; Sedova, Ksenia A.; et al.; Blockade of melatonin receptors abolishes its antiarrhythmic effect and slows ventricular conduction in rat hearts; Molecular Diversity Preservation International; International Journal of Molecular Sciences; 24; 15; 8-2023; 1-16
1661-6596
1422-0067
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/1422-0067/24/15/11931
info:eu-repo/semantics/altIdentifier/doi/10.3390/ijms241511931
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Molecular Diversity Preservation International
publisher.none.fl_str_mv Molecular Diversity Preservation International
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.13397

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