ArticleBasic research in cardiology2016
Persistent increases in Ca(2+) influx through Cav1.2 shortens action potential and causes Ca(2+) overload-induced afterdepolarizations and arrhythmias.
Article in Basic research in cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
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- Protein Kinase A Is a Master Regulator of Physiological and Pathological Cardiac Hypertrophy.Circulation research · 2024Article
- Rapid Pacing Decreases L-type CaThe Journal of membrane biology · 2023Article
- Sympathetic Nervous System Regulation of Cardiac Calcium Channels.Handbook of experimental pharmacology · 2023Article
- Regulation of Papillary Muscle Contractility by NAD and Ammonia Interplay: Contribution of Ion Channels and Exchangers.Membranes · 2022Article
- Antiepileptic Drug Tiagabine Does Not Directly Target Key Cardiac Ion Channels Kv11.1, Nav1.5 and Cav1.2.Molecules (Basel, Switzerland) · 2021Article
- Evidence of Ventricular Arrhythmogenicity and Cardiac Sympathetic Hyperinnervation in Early Cirrhotic Cardiomyopathy.Frontiers in physiology · 2021Article
- Chromatin compartment dynamics in a haploinsufficient model of cardiac laminopathy.The Journal of cell biology · 2019Article
- Augmentation of myocardial INature communications · 2019Article
- Barbaloin inhibits ventricular arrhythmias in rabbits by modulating voltage-gated ion channels.Acta pharmacologica Sinica · 2018Article
- Effect of ovariectomy on intracellular CaAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Remodeling of repolarization and arrhythmia susceptibility in a myosin-binding protein C knockout mouse model.American journal of physiology. Heart and circulatory physiology · 2017Article
- The role of spatial organization of CaBasic research in cardiology · 2017Article
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- Cardiac expression of the CREM repressor isoform CREM-IbΔC-X in mice leads to arrhythmogenic alterations in ventricular cardiomyocytes.Basic research in cardiology · 2016Article
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
Persistent elevation of Ca(2+) influx due to prolongation of the action potential (AP), chronic activation of the β-adrenergic system and molecular remodeling occurs in stressed and diseased hearts. Increases in Ca(2+) influx are usually linked to prolonged myocyte action potentials and arrhythmias. However, the contribution of chronic enhancement of Cav1.2 activity on cardiac electrical remodeling and arrhythmogenicity has not been completely defined and is the subject of this study. Chronically increased Cav1.2 activity was produced with a cardiac specific, inducible double transgenic (DTG) mouse system overexpressing the β2a subunit of Cav (Cavβ2a). DTG myocytes had increased L-type Ca(2+) current (ICa-L), myocyte shortening, and Ca(2+) transients. DTG mice had enhanced cardiac performance, but died suddenly and prematurely. Telemetric electrocardiograms revealed shortened QT intervals in DTG mice. The action potential duration (APD) was shortened in DTG myocytes due to significant increases of potassium currents and channel abundance. However, shortened AP in DTG myocytes did not fully limit excess Ca(2+) influx and increased the peak and tail ICa-L. Enhanced ICa promoted sarcoplasmic reticulum (SR) Ca(2+) overload, diastolic Ca(2+) sparks and waves, and increased NCX activity, causing increased occurrence of early and delayed afterdepolarizations (EADs and DADs) that may contribute to premature ventricular beats and ventricular tachycardia. AV blocks that could be related to fibrosis of the AV node were also observed. Our study suggests that increasing ICa-L does not necessarily result in AP prolongation but causes SR Ca(2+) overload and fibrosis of AV node and myocardium to induce cellular arrhythmogenicity, arrhythmias, and conduction abnormalities.
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