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Differential Modulation of I-K and I-Ca,I-L Channels in High-Fat Diet-Induced Obese Guinea Pig Atria

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Differential Modulation of I-K and I-Ca,I-L Channels in High-Fat Diet-Induced Obese Guinea Pig Atria

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dc.contributor.author Martínez-Mateu, Laura es_ES
dc.contributor.author Saiz Rodríguez, Francisco Javier es_ES
dc.contributor.author Aromolaran, Ademuyiwa S. es_ES
dc.date.accessioned 2020-06-06T03:32:32Z
dc.date.available 2020-06-06T03:32:32Z
dc.date.issued 2019-09-25 es_ES
dc.identifier.issn 1664-042X es_ES
dc.identifier.uri http://hdl.handle.net/10251/145544
dc.description.abstract [EN] Obesity mechanisms that make atrial tissue vulnerable to arrhythmia are poorly understood. Voltage-dependent potassium (I-K, I-Kur, and I-K1) and L-type calcium currents (I-Ca,I- L) are electrically relevant and represent key substrates for modulation in obesity. We investigated whether electrical remodeling produced by high-fat diet (HFD) alone or in concert with acute atrial stimulation were different. Electrophysiology was used to assess atrial electrical function after short-term HFD-feeding in guinea pigs. HFD atria displayed spontaneous beats, increased I-K (I-Kr + I-Ks) and decreased I-Ca,I- L densities. Only with pacing did a reduction in I-Kur and increased I-K1 phenotype emerge, leading to a further shortening of action potential duration. Computer modeling studies further indicate that the measured changes in potassium and calcium current densities contribute prominently to shortened atrial action potential duration in human heart. Our data are the first to show that multiple mechanisms (shortened action potential duration, early after depolarizations and increased incidence of spontaneous beats) may underlie initiation of supraventricular arrhythmias in obese guinea pig hearts. These results offer different mechanistic insights with implications for obese patients harboring supraventricular arrhythmias. es_ES
dc.description.sponsorship This study was supported by an AHA (13SDG16850065 to AA), NIH (R01 HL147044 to AA), and Programa Prometeu de la Conselleria d Educació, Formació I Ocupació de la Generalitat Valenciana, award number PROMETEU/2016/088. es_ES
dc.language Inglés es_ES
dc.publisher Frontiers Media SA es_ES
dc.relation.ispartof Frontiers in Physiology es_ES
dc.rights Reconocimiento (by) es_ES
dc.subject High-fat diet es_ES
dc.subject HERG es_ES
dc.subject KCNQ1 es_ES
dc.subject Cardiomyocytes es_ES
dc.subject Guinea pig es_ES
dc.subject Atria es_ES
dc.subject.classification TECNOLOGIA ELECTRONICA es_ES
dc.title Differential Modulation of I-K and I-Ca,I-L Channels in High-Fat Diet-Induced Obese Guinea Pig Atria es_ES
dc.type Artículo es_ES
dc.identifier.doi 10.3389/fphys.2019.01212 es_ES
dc.relation.projectID info:eu-repo/grantAgreement/AHA//13SDG16850065/ es_ES
dc.relation.projectID info:eu-repo/grantAgreement/NIH//R01HL147044/ es_ES
dc.relation.projectID info:eu-repo/grantAgreement/GVA//PROMETEO%2F2016%2F088/ES/MODELOS COMPUTACIONALES PERSONALIZADOS MULTI-ESCALA PARA LA OPTIMIZACION DEL DIAGNOSTICO Y TRATAMIENTO DE ARRITMIAS CARDIACAS (PERSONALISED DIGITAL HEART)/ es_ES
dc.rights.accessRights Abierto es_ES
dc.contributor.affiliation Universitat Politècnica de València. Departamento de Ingeniería Electrónica - Departament d'Enginyeria Electrònica es_ES
dc.description.bibliographicCitation Martínez-Mateu, L.; Saiz Rodríguez, FJ.; Aromolaran, A. (2019). Differential Modulation of I-K and I-Ca,I-L Channels in High-Fat Diet-Induced Obese Guinea Pig Atria. Frontiers in Physiology. 10:1-18. https://doi.org/10.3389/fphys.2019.01212 es_ES
dc.description.accrualMethod S es_ES
dc.relation.publisherversion https://doi.org/10.3389/fphys.2019.01212 es_ES
dc.description.upvformatpinicio 1 es_ES
dc.description.upvformatpfin 18 es_ES
dc.type.version info:eu-repo/semantics/publishedVersion es_ES
dc.description.volume 10 es_ES
dc.identifier.pmid 31607952 es_ES
dc.identifier.pmcid PMC6773813 es_ES
dc.relation.pasarela S\400326 es_ES
dc.contributor.funder Generalitat Valenciana es_ES
dc.contributor.funder American Heart Association es_ES
dc.contributor.funder National Institutes of Health, EEUU es_ES
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