ArticleThe Journal of physiology2004
Mice overexpressing the cardiac sodium-calcium exchanger: defects in excitation-contraction coupling.
Article in The Journal of physiology, 2004. 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, 52 citations in OpenAlex.
- Cardiac TRPV1 afferent signaling promotes arrhythmogenic ventricular remodeling after myocardial infarction.JCI insight · 2020Article
- Small and Intermediate Calcium Activated Potassium Channels in the Heart: Role and Strategies in the Treatment of Cardiovascular Diseases.Frontiers in physiology · 2020Review
- Pathophysiology of Calcium Mediated Ventricular Arrhythmias and Novel Therapeutic Options with Focus on Gene Therapy.International journal of molecular sciences · 2019Review
- Triggered activity in atrial myocytes is influenced by NaJournal of molecular and cellular cardiology · 2016Article
- Pivotal role of α2 NaThe Journal of physiology · 2016Review
- Mitochondrial Ca(2+) uptake by the voltage-dependent anion channel 2 regulates cardiac rhythmicity.eLife · 2015Article
- Na/Ca exchange and contraction of the heart.Journal of molecular and cellular cardiology · 2013Review
- MicroRNA-214 protects the mouse heart from ischemic injury by controlling Ca²⁺ overload and cell death.The Journal of clinical investigation · 2012Article
- Proarrhythmia in a non-failing murine model of cardiac-specific Na+/Ca 2+ exchanger overexpression: whole heart and cellular mechanisms.Basic research in cardiology · 2012Article
- Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice.The Journal of clinical investigation · 2012Article
- Ca2+-calmodulin-dependent protein kinase II represses cardiac transcription of the L-type calcium channel alpha(1C)-subunit gene (Cacna1c) by DREAM translocation.The Journal of physiology · 2011Article
- Chromatin remodelling complex dosage modulates transcription factor function in heart development.Nature communications · 2011Article
- Chronic administration of KB-R7943 induces up-regulation of cardiac NCX1.The Journal of biological chemistry · 2009Article
- Induced overexpression of Na+/Ca2+ exchanger transgene: altered myocyte contractility, [Ca2+]i transients, SR Ca2+ contents, and action potential duration.American journal of physiology. Heart and circulatory physiology · 2009Article
- On the physiological roles of PIP(2) at cardiac Na+ Ca2+ exchangers and K(ATP) channels: a long journey from membrane biophysics into cell biology.The Journal of physiology · 2007Article
- Hypertrophy and heart failure in mice overexpressing the cardiac sodium-calcium exchanger.Journal of cardiac failure · 2007Article
- Contribution of the Na+/Ca2+ exchanger to rapid Ca2+ release in cardiomyocytes.Biophysical journal · 2006Article
- Excitation-contraction coupling in Na+-Ca2+ exchanger knockout mice: reduced transsarcolemmal Ca2+ flux.Circulation research · 2005Article
- Mutation in sodium-calcium exchanger 1 (NCX1) causes cardiac fibrillation in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- The L-type calcium channel in the heart: the beat goes on.The Journal of clinical investigation · 2005Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Homozygous overexpression of the cardiac Na(+)-Ca(2+) exchanger causes cardiac hypertrophy and increases susceptibility to heart failure in response to stress. We studied the functional effects of homozygous overexpression of the exchanger at the cellular level in isolated mouse ventricular myocytes. Compared with patch-clamped myocytes from wild-type animals, non-failing myocytes from homozygous transgenic mice exhibited increased cell capacitance (from 208 +/- 16 pF to 260 +/- 15 pF, P < 0.05). Intracellular Ca(2+) oscillations were readily elicited in homozygous transgenic animals during depolarizations to +80 mV, consistent with rapid Ca(2+) overload caused by reverse Na(+)-Ca(2+) exchange. After normalization to cell capacitance, transgenic myocytes had significant increases in Na(+)-Ca(2+) exchange activity (318%) and peak L-type Ca(2+) current (8.2 +/- 0.7 pA pF(-1) at 0 mV test potential) compared to wild-type (5.8 +/- 0.9 pA pF(-1) at 0 mV, P < 0.02). The peak Ca(2+) current amplitude and its rate of inactivation could be modulated by rapid reversible block of the exchanger. Thus, we describe an unexpected direct influence of Na(+)-Ca(2+) exchange activity on the L-type Ca(2+) channel. Despite intact sarcoplasmic reticular Ca(2+) content and larger peak L-type Ca(2+) currents, homozygous transgenic animals exhibited smaller Ca(2+) transients (Delta[Ca(2+)](i)= 466 +/- 48 nm in transgenics versus 892 +/- 104 nm in wild-type, P < 0.0005) and substantially reduced gain of excitation-contraction coupling. These alterations in excitation-contraction coupling may underlie the tendency for these animals to develop heart failure following haemodynamic stress.
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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.