ArticleCirculation research2005
Excitation-contraction coupling in Na+-Ca2+ exchanger knockout mice: reduced transsarcolemmal Ca2+ flux.
Article in Circulation research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
50 citing papers in PubMed, 99 citations in OpenAlex.
- Regulation of Na/Ca exchange by cytoplasmic protons modifies intracellular calcium dynamics and the cardiac response to ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Hypercontractile cardiac phenotype in mice overexpressing the regulatory subunit PR72 of protein phosphatase 2A.Frontiers in cardiovascular medicine · 2023Article
- Regulation of APD and Force by the NaCells · 2022Article
- Mutation in RyR2-FKBP Binding site alters CaCell calcium · 2022Article
- Acute Genetic Ablation of Cardiac Sodium/Calcium Exchange in Adult Mice: Implications for Cardiomyocyte Calcium Regulation, Cardioprotection, and Arrhythmia.Journal of the American Heart Association · 2021Article
- Intracellular NaInternational journal of molecular sciences · 2021Article
- Sarcoplasmic Reticulum Calcium Release Is Required for Arrhythmogenesis in the Mouse.Frontiers in physiology · 2021Article
- Na/Ca exchange in the atrium: Role in sinoatrial node pacemaking and excitation-contraction coupling.Cell calcium · 2020Review
- The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications.Circulation research · 2020Review
- Action Potential Shortening and Impairment of Cardiac Function by Ablation ofCirculation. Arrhythmia and electrophysiology · 2017Article
- The Effects of SEA0400 on CaFrontiers in pharmacology · 2017Article
- Triggered activity in atrial myocytes is influenced by NaJournal of molecular and cellular cardiology · 2016Article
- Intact Heart Loose Patch Photolysis Reveals Ionic Current Kinetics During Ventricular Action Potentials.Circulation research · 2016Article
- Article
- Regulation of calcium clock-mediated pacemaking by inositol-1,4,5-trisphosphate receptors in mouse sinoatrial nodal cells.The Journal of physiology · 2015Article
- Eps15 Homology Domain-containing Protein 3 Regulates Cardiac T-type Ca2+ Channel Targeting and Function in the Atria.The Journal of biological chemistry · 2015Article
- Na+/Ca2+ exchange and Na+/K+-ATPase in the heart.The Journal of physiology · 2015Review
- Endosome-based protein trafficking and Ca(2+) homeostasis in the heart.Frontiers in physiology · 2015Review
- Overexpression of junctophilin-2 does not enhance baseline function but attenuates heart failure development after cardiac stress.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac-specific Na+-Ca2+ exchanger (NCX) knockout (KO) mice surprisingly survive into adulthood without compensatory changes in protein expression levels. To determine how cardiac function is maintained in the absence of NCX, we investigated membrane currents, intracellular Ca2+, and action potentials (APs) in whole cell patch-clamped myocytes from wild-type (WT) and NCX knockout mice. There was no difference in resting Ca2+ or sarcoplasmic reticular Ca2+ load between KO and WT. During prolonged caffeine exposure, the decrease of the Ca2+ transient was drastically slowed in KO versus WT myocytes, indicating that no alternative Ca2+-extrusion mechanism is upregulated to compensate for the absence of NCX. Peak L-type Ca2+ current (ICa) was reduced by 62% in KO myocytes compared with WT. Nevertheless, the corresponding Ca2+ transients were similar, implying an increase in the gain of excitation-contraction coupling in KO cells. APs recorded from KO cells repolarized more rapidly than in WT. In WT myocytes, applying a KO AP waveform voltage clamp reduced Ca2+ influx via ICa by 59% compared with WT AP waveform clamps. Again, the corresponding Ca2+ transients remained similar. Our findings indicate that NCX KO myocytes limit Ca2+ influx to &20% of that in WT by reducing ICa and by abbreviating the AP. Contractility is maintained by an increase in the gain of excitation-contraction coupling resulting from both a more rapid repolarization of the AP and an as yet unidentified AP-independent mechanism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.