LIVIVO - Search results -

Search results

Result 1 - 10 of total 117

Search options

Article: Acute Detubulation of Ventricular Myocytes Amplifies the Inhibitory Effect of Cholinergic Agonist on Intracellular Ca

Belevych, Andriy E / Bogdanov, Vladimir / Terentyev, Dmitry A / Gyorke, Sandor

2021 Volume 12, Page(s) 725798

Abstract: Muscarinic receptors expressed in cardiac myocytes play a critical role in the regulation of heart function by the parasympathetic nervous system. How the structural organization of cardiac myocytes affects the regulation of ... ...

Abstract	Muscarinic receptors expressed in cardiac myocytes play a critical role in the regulation of heart function by the parasympathetic nervous system. How the structural organization of cardiac myocytes affects the regulation of Ca
Language	English
Publishing date	2021-08-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.725798
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: Molecular basis of catecholaminergic polymorphic ventricular tachycardia.

Györke, Sandor

Heart rhythm

2009 Volume 6, Issue 1, Page(s) 123–129

Abstract: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a malignant arrhythmia syndrome linked to mutations in the cardiac ryanodine receptor (RyR2) and calsequestrin (CASQ2). RyR2 and CASQ2 are parts of the multimolecular Ca(2+) release channel ... ...

Abstract	Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a malignant arrhythmia syndrome linked to mutations in the cardiac ryanodine receptor (RyR2) and calsequestrin (CASQ2). RyR2 and CASQ2 are parts of the multimolecular Ca(2+) release channel complex that is present on the sarcoplasmic reticulum (SR) to support myocyte Ca(2+) cycling and contractile activity. Whereas RyR2 operates as a Ca(2+) release channel, the SR Ca(2+) binding protein CASQ2 plays a dual role by serving as a SR Ca(2+) buffer and by regulating RyR2 function. Essential to stable Ca(2+) cycling, SR luminal Ca(2+)-dependent control of RyR2 activity by CASQ2 contributes to RyR2 deactivation and to the development of a temporary refractory state that occurs after each Ca(2+) release. Accumulating evidence suggests that the CPVT mutations act by reducing the extent and shortening the duration of Ca(2+) signaling refractoriness, thereby promoting untimely SR Ca(2+) release and arrhythmogenic delayed afterdepolarizations in cardiac myocytes. Similar mechanisms may apply to arrhythmias during various conditions, including heart failure and ischemic heart disease, associated with acquired defects in components of the Ca(2+) release channel complex.
MeSH term(s)	Calcium/metabolism ; Calcium Channels/metabolism ; Catecholamines/metabolism ; Humans ; Intracellular Fluid/metabolism ; Myocardium/metabolism ; Signal Transduction ; Tachycardia, Ventricular/metabolism
Chemical Substances	Calcium Channels ; Catecholamines ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2009-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2229357-7
ISSN	1556-3871 ; 1547-5271
ISSN (online)	1556-3871
ISSN	1547-5271
DOI	10.1016/j.hrthm.2008.09.013
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6278: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Neuronal sodium channels: emerging components of the nano-machinery of cardiac calcium cycling.

Veeraraghavan, Rengasayee / Györke, Sándor / Radwański, Przemysław B

The Journal of physiology

2017 Volume 595, Issue 12, Page(s) 3823–3834

Abstract: Excitation-contraction coupling is the bridge between cardiac electrical activation and mechanical contraction. It is driven by the influx of ... ...

Abstract	Excitation-contraction coupling is the bridge between cardiac electrical activation and mechanical contraction. It is driven by the influx of Ca
MeSH term(s)	Action Potentials/physiology ; Animals ; Arrhythmias, Cardiac/metabolism ; Calcium/metabolism ; Excitation Contraction Coupling/physiology ; Humans ; Myocytes, Cardiac/metabolism ; Neurons/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sodium/metabolism ; Sodium Channels/metabolism
Chemical Substances	Sodium Channels ; Sodium (9NEZ333N27) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2017-03-26
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP273058
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uc I Zs.65: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Cardiac Arrhythmias as Manifestations of Nanopathies: An Emerging View.

Radwański, Przemysław B / Johnson, Christopher N / Györke, Sándor / Veeraraghavan, Rengasayee

Frontiers in physiology

2018 Volume 9, Page(s) 1228

Abstract: A nanodomain is a collection of proteins localized within a specialized, nanoscale structural environment, which can serve as the functional unit of macroscopic physiologic processes. We are beginning to recognize the key roles of cardiomyocyte ... ...

Abstract	A nanodomain is a collection of proteins localized within a specialized, nanoscale structural environment, which can serve as the functional unit of macroscopic physiologic processes. We are beginning to recognize the key roles of cardiomyocyte nanodomains in essential processes of cardiac physiology such as electrical impulse propagation and excitation-contraction coupling (ECC). There is growing appreciation of nanodomain dysfunction, i.e., nanopathy, as a mechanistic driver of life-threatening arrhythmias in a variety of pathologies. Here, we offer an overview of current research on the role of nanodomains in cardiac physiology with particular emphasis on: (1) sodium channel-rich nanodomains within the intercalated disk that participate in cell-to-cell electrical coupling and (2) dyadic nanodomains located along transverse tubules that participate in ECC. The beat to beat function of cardiomyocytes involves three phases: the action potential, the calcium transient, and mechanical contraction/relaxation. In all these phases, cell-wide function results from the aggregation of the stochastic function of individual proteins. While it has long been known that proteins that exist in close proximity influence each other's function, it is increasingly appreciated that there exist nanoscale structures that act as functional units of cardiac biophysical phenomena. Termed nanodomains, these structures are collections of proteins, localized within specialized nanoscale structural environments. The nano-environments enable the generation of localized electrical and/or chemical gradients, thereby conferring unique functional properties to these units. Thus, the function of a nanodomain is determined by its protein constituents as well as their local structural environment, adding an additional layer of complexity to cardiac biology and biophysics. However, with the emergence of experimental techniques that allow direct investigation of structure and function at the nanoscale, our understanding of cardiac physiology and pathophysiology at these scales is rapidly advancing. Here, we will discuss the structure and functions of multiple cardiomyocyte nanodomains, and novel strategies that target them for the treatment of cardiac arrhythmias.
Language	English
Publishing date	2018-09-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2018.01228
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: NaV1.6 dysregulation within myocardial T-tubules by D96V calmodulin enhances proarrhythmic sodium and calcium mishandling.

Tarasov, Mikhail / Struckman, Heather L / Olgar, Yusuf / Miller, Alec / Demirtas, Mustafa / Bogdanov, Vladimir / Terentyeva, Radmila / Soltisz, Andrew M / Meng, Xiaolei / Min, Dennison / Sakuta, Galina / Dunlap, Izabella / Duran, Antonia D / Foster, Mark P / Davis, Jonathan P / Terentyev, Dmitry / Györke, Sándor / Veeraraghavan, Rengasayee / Radwański, Przemysław B

The Journal of clinical investigation

2023 Volume 133, Issue 7

Abstract: Calmodulin (CaM) plays critical roles in cardiomyocytes, regulating Na+ (NaV) and L-type Ca2+ channels (LTCCs). LTCC dysregulation by mutant CaMs has been implicated in action potential duration (APD) prolongation and arrhythmogenic long QT (LQT) ... ...

Abstract	Calmodulin (CaM) plays critical roles in cardiomyocytes, regulating Na+ (NaV) and L-type Ca2+ channels (LTCCs). LTCC dysregulation by mutant CaMs has been implicated in action potential duration (APD) prolongation and arrhythmogenic long QT (LQT) syndrome. Intriguingly, D96V-CaM prolongs APD more than other LQT-associated CaMs despite inducing comparable levels of LTCC dysfunction, suggesting dysregulation of other depolarizing channels. Here, we provide evidence implicating NaV dysregulation within transverse (T) tubules in D96V-CaM-associated arrhythmias. D96V-CaM induced a proarrhythmic late Na+ current (INa) by impairing inactivation of NaV1.6, but not the predominant cardiac NaV isoform NaV1.5. We investigated arrhythmia mechanisms using mice with cardiac-specific expression of D96V-CaM (cD96V). Super-resolution microscopy revealed close proximity of NaV1.6 and RyR2 within T-tubules. NaV1.6 density within these regions increased in cD96V relative to WT mice. Consistent with NaV1.6 dysregulation by D96V-CaM in these regions, we observed increased late NaV activity in T-tubules. The resulting late INa promoted aberrant Ca2+ release and prolonged APD in myocytes, leading to LQT and ventricular tachycardia in vivo. Cardiac-specific NaV1.6 KO protected cD96V mice from increased T-tubular late NaV activity and its arrhythmogenic consequences. In summary, we demonstrate that D96V-CaM promoted arrhythmias by dysregulating LTCCs and NaV1.6 within T-tubules and thereby facilitating aberrant Ca2+ release.
MeSH term(s)	Mice ; Animals ; Calmodulin/genetics ; Calmodulin/metabolism ; Calcium/metabolism ; Sodium/metabolism ; Arrhythmias, Cardiac/genetics ; Arrhythmias, Cardiac/metabolism ; Long QT Syndrome/genetics ; Myocytes, Cardiac/metabolism ; NAV1.5 Voltage-Gated Sodium Channel/genetics
Chemical Substances	Calmodulin ; Calcium (SY7Q814VUP) ; Sodium (9NEZ333N27) ; NAV1.5 Voltage-Gated Sodium Channel
Language	English
Publishing date	2023-04-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI152071
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ua VI Zs.184: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: STIM1 ablation impairs exercise-induced physiological cardiac hypertrophy and dysregulates autophagy in mouse hearts.

Bonilla, Ingrid M / Baine, Stephen / Pokrass, Anastasia / Mariángelo, Juan Ignacio Elio / Kalyanasundaram, Anuradha / Bogdanov, Vladimir / Mezache, Louisa / Sakuta, Galina / Beard, Casey M / Belevych, Andriy / Tikunova, Svetlana / Terentyeva, Radmila / Terentyev, Dmitry / Davis, Jonathan / Veeraraghavan, Rengasayee / Carnes, Cynthia A / Györke, Sandor

Journal of applied physiology (Bethesda, Md. : 1985)

2023 Volume 134, Issue 5, Page(s) 1287–1299

Abstract: Cardiac stromal interaction molecule 1 (STIM1), a key mediator of store-operated ... ...

Abstract	Cardiac stromal interaction molecule 1 (STIM1), a key mediator of store-operated Ca
MeSH term(s)	Mice ; Animals ; Myocytes, Cardiac/metabolism ; Calcium Channels/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Stromal Interaction Molecule 1/metabolism ; Cardiomegaly/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Mice, Knockout ; Calcium/metabolism ; Calcium Signaling ; Mammals/metabolism
Chemical Substances	Calcium Channels ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Stromal Interaction Molecule 1 ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Calcium (SY7Q814VUP) ; Stim1 protein, mouse
Language	English
Publishing date	2023-03-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.00363.2022
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.249: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Ero1α-Dependent ERp44 Dissociation From RyR2 Contributes to Cardiac Arrhythmia.

Hamilton, Shanna / Terentyeva, Radmila / Bogdanov, Vladimir / Kim, Tae Yun / Perger, Fruzsina / Yan, Jiajie / Ai, Xun / Carnes, Cynthia A / Belevych, Andriy E / George, Christopher H / Davis, Jonathan P / Gyorke, Sandor / Choi, Bum-Rak / Terentyev, Dmitry

Circulation research

2022 Volume 130, Issue 5, Page(s) 711–724

Abstract: Background: Oxidative stress in cardiac disease promotes proarrhythmic disturbances in Ca: Methods: A rat model of hypertrophy induced by thoracic aortic banding (TAB) was used for ex vivo whole heart optical mapping and for Ca: Results: The SR- ... ...

Abstract	Background: Oxidative stress in cardiac disease promotes proarrhythmic disturbances in Ca Methods: A rat model of hypertrophy induced by thoracic aortic banding (TAB) was used for ex vivo whole heart optical mapping and for Ca Results: The SR-targeted reactive oxygen species biosensor ERroGFP showed increased intra-SR oxidation in TAB VMs that was associated with increased expression of Ero1α (endoplasmic reticulum oxidoreductase 1 alpha). Pharmacological (EN460) or genetic Ero1α inhibition normalized SR redox state, increased Ca Conclusions: A novel axis of intraluminal interaction between RyR2, ERp44, and Ero1α has been identified. Ero1α inhibition exhibits promising therapeutic potential by stabilizing RyR2-ERp44 complex, thereby reducing spontaneous Ca
MeSH term(s)	Animals ; Arrhythmias, Cardiac/metabolism ; Calcium/metabolism ; Calcium Signaling ; Heart Diseases/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Isoproterenol/pharmacology ; Membrane Glycoproteins/metabolism ; Myocytes, Cardiac/metabolism ; Oxidoreductases/metabolism ; Oxidoreductases/pharmacology ; Rats ; Reactive Oxygen Species/metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/metabolism
Chemical Substances	Ero1a protein, rat ; Erp44 protein, rat ; Intracellular Signaling Peptides and Proteins ; Membrane Glycoproteins ; Reactive Oxygen Species ; RyR2 protein, rat ; Ryanodine Receptor Calcium Release Channel ; Oxidoreductases (EC 1.-) ; Isoproterenol (L628TT009W) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.121.320531
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui IV Zs.70: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Ui IV Zs.60: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Vascular endothelial growth factor promotes atrial arrhythmias by inducing acute intercalated disk remodeling.

Mezache, Louisa / Struckman, Heather L / Greer-Short, Amara / Baine, Stephen / Györke, Sándor / Radwański, Przemysław B / Hund, Thomas J / Veeraraghavan, Rengasayee

Scientific reports

2020 Volume 10, Issue 1, Page(s) 20463

Abstract: Atrial fibrillation (AF) is the most common arrhythmia and is associated with inflammation. AF patients have elevated levels of inflammatory cytokines known to promote vascular leak, such as vascular endothelial growth factor A (VEGF). However, the ... ...

Abstract	Atrial fibrillation (AF) is the most common arrhythmia and is associated with inflammation. AF patients have elevated levels of inflammatory cytokines known to promote vascular leak, such as vascular endothelial growth factor A (VEGF). However, the contribution of vascular leak and consequent cardiac edema to the genesis of atrial arrhythmias remains unknown. Previous work suggests that interstitial edema in the heart can acutely promote ventricular arrhythmias by disrupting ventricular myocyte intercalated disk (ID) nanodomains rich in cardiac sodium channels (Na
MeSH term(s)	Animals ; Atrial Fibrillation/metabolism ; Atrial Fibrillation/physiopathology ; Electrocardiography ; Gap Junctions/metabolism ; Heart Conduction System/drug effects ; Heart Conduction System/metabolism ; Heart Conduction System/physiopathology ; Male ; Mice ; Microscopy, Electron, Transmission ; Models, Biological ; NAV1.5 Voltage-Gated Sodium Channel/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factors/pharmacology
Chemical Substances	NAV1.5 Voltage-Gated Sodium Channel ; Scn5a protein, mouse ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; vascular endothelial growth factor A, mouse
Language	English
Publishing date	2020-11-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-77562-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Conditional Up-Regulation of SERCA2a Exacerbates RyR2-Dependent Ventricular and Atrial Arrhythmias.

Liu, Bin / Lou, Qing / Smith, Heather / Velez-Cortes, Florencia / Dillmann, Wolfgang H / Knollmann, Björn C / Armoundas, Antonis A / Györke, Sándor

International journal of molecular sciences

2020 Volume 21, Issue 7

Abstract: Ryanodine receptor 2 (RyR2) and SERCA2a are two major players in myocyte calcium (Ca) cycling that are modulated physiologically, affected by disease and thus considered to be potential targets for cardiac disease therapy. However, how RyR2 and SERCA2a ... ...

Abstract	Ryanodine receptor 2 (RyR2) and SERCA2a are two major players in myocyte calcium (Ca) cycling that are modulated physiologically, affected by disease and thus considered to be potential targets for cardiac disease therapy. However, how RyR2 and SERCA2a influence each others' activities, as well as the primary and secondary consequences of their combined manipulations remain controversial. In this study, we examined the effect of acute upregulation of SERCA2a on arrhythmogenesis by conditionally overexpressing SERCA2a in a mouse model featuring hyperactive RyR2s due to ablation of calsequestrin 2 (CASQ2). CASQ2 knock-out (KO) mice were crossbred with doxycycline (DOX)-inducible SERCA2a transgenic mice to generate KO-TG mice. In-vivo ECG studies have shown that induction of SERCA2a (DOX+) overexpression markedly exacerbated both ventricular and atrial arrhythmias in vivo, compared with uninduced KO-TG mice (DOX-). Consistent with that, confocal microscopy in both atrial and ventricular myocytes demonstrated that conditional upregulation of SERCA2a enhanced the rate of occurrence of diastolic Ca release events. Additionally, deep RNA sequencing identified 17 downregulated genes and 5 upregulated genes in DOX+ mice, among which Ppp1r13l, Clcn1, and Agt have previously been linked to arrhythmias. Our results suggest that conditional upregulation of SERCA2a exacerbates hyperactive RyR2-mediated arrhythmias by further elevating diastolic Ca release.
MeSH term(s)	Action Potentials ; Animals ; Arrhythmias, Cardiac/genetics ; Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/physiopathology ; Calcium Signaling ; Calsequestrin/genetics ; Cells, Cultured ; Heart Atria/cytology ; Heart Atria/metabolism ; Heart Atria/physiopathology ; Heart Ventricles/cytology ; Heart Ventricles/metabolism ; Heart Ventricles/physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/physiology ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/genetics ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Transcriptome ; Up-Regulation
Chemical Substances	Calsequestrin ; Ryanodine Receptor Calcium Release Channel ; casq2 protein, mouse ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8) ; Atp2a2 protein, mouse (EC 7.2.2.10)
Language	English
Publishing date	2020-04-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21072535
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Accentuated vagal antagonism paradoxically increases ryanodine receptor calcium leak in long-term exercised Calsequestrin2 knockout mice.

Ho, Hsiang-Ting / Thambidorai, Senthil / Knollmann, Björn C / Billman, George E / Györke, Sandor / Kalyanasundaram, Anuradha

Heart rhythm

2017 Volume 15, Issue 3, Page(s) 430–441

Abstract: Background: Long-term aerobic exercise alters autonomic balance, which may not be favorable in heart rate (HR)-dependent arrhythmic diseases including catecholaminergic polymorphic ventricular tachycardia (CPVT) because of preexisting bradycardia and ... ...

Abstract	Background: Long-term aerobic exercise alters autonomic balance, which may not be favorable in heart rate (HR)-dependent arrhythmic diseases including catecholaminergic polymorphic ventricular tachycardia (CPVT) because of preexisting bradycardia and increased sensitivity to parasympathetic stimulation. Objective: The purpose of this study was to determine whether long-term exercise-induced autonomic adaptations modify CPVT susceptibility. Methods: We determined exercise-induced parasympathetic effects on HR, arrhythmia incidence, and intracellular sarcoplasmic reticulum (SR) Ca Results: Although 8-week treadmill running improved exercise capacity in EX CPVT mice, the incidence and duration of ventricular tachycardia also increased. HR variability analyses revealed an increased high-frequency component of the power spectrum and root mean square of successive differences in R-R intervals indicating accentuated vagal antagonism during β-adrenergic stimulation resulting in negligible HR acceleration. In EX CASQ2 Conclusion: Our novel results suggest that long-term exercise in CASQ2
MeSH term(s)	Animals ; Calsequestrin/metabolism ; Disease Models, Animal ; Follow-Up Studies ; Male ; Mice ; Mice, Knockout ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Physical Conditioning, Animal ; Ryanodine Receptor Calcium Release Channel/metabolism ; Tachycardia, Ventricular/metabolism ; Tachycardia, Ventricular/pathology ; Tachycardia, Ventricular/physiopathology ; Time Factors ; Vagus Nerve/physiopathology
Chemical Substances	Calsequestrin ; Ryanodine Receptor Calcium Release Channel ; casq2 protein, mouse
Language	English
Publishing date	2017-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2229357-7
ISSN	1556-3871 ; 1547-5271
ISSN (online)	1556-3871
ISSN	1547-5271
DOI	10.1016/j.hrthm.2017.10.008
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6278: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito