ArticleThe Journal of physiology2010
Na+ currents are required for efficient excitation-contraction coupling in rabbit ventricular myocytes: a possible contribution of neuronal Na+ channels.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 50 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
- A Possible Role of Tetrodotoxin-Sensitive NaInternational journal of molecular sciences · 2024Article
- Pharmacological characterization of crotamine effects on mice hind limb paralysis employing both ex vivo and in vivo assays: Insights into the involvement of voltage-gated ion channels in the crotamine action on skeletal muscles.PLoS neglected tropical diseases · 2018Article
- A privileged role for neuronal NaThe Journal of general physiology · 2018Article
- Tetrodotoxin-sensitive NaThe Journal of general physiology · 2018Article
- Cardiac Arrhythmias as Manifestations of Nanopathies: An Emerging View.Frontiers in physiology · 2018Review
- Neuronal sodium channels: emerging components of the nano-machinery of cardiac calcium cycling.The Journal of physiology · 2017Review
- Sensitized signalling between L-type Ca2+ channels and ryanodine receptors in the absence or inhibition of FKBP12.6 in cardiomyocytes.Cardiovascular research · 2017Article
- Species-Dependent Mechanisms of Cardiac Arrhythmia: A Cellular Focus.Clinical Medicine Insights. Cardiology · 2017Review
- Cardiac arrhythmia in a mouse model of sodium channelProceedings of the National Academy of Sciences of the United States of America · 2016Article
- Modeling NaJournal of molecular and cellular cardiology · 2016Article
- Neuronal NaJACC. Basic to translational science · 2016Article
- Neuronal Na+ channel blockade suppresses arrhythmogenic diastolic Ca2+ release.Cardiovascular research · 2015Article
- Na+/Ca2+ exchange and Na+/K+-ATPase in the heart.The Journal of physiology · 2015Review
- Distinguishing between overdrive excited and suppressed ventricular beats in guinea pig ventricular myocardium.Frontiers in physiology · 2015Article
- Junctional cleft [Ca²⁺]i measurements using novel cleft-targeted Ca²⁺ sensors.Circulation research · 2014Article
- Decreased cardiac excitability secondary to reduction of sodium current may be a significant contributor to reduced contractility in a rat model of sepsis.Critical care (London, England) · 2014Article
- Localization of sodium channel subtypes in mouse ventricular myocytes using quantitative immunocytochemistry.Journal of molecular and cellular cardiology · 2013Article
- Na/Ca exchange and contraction of the heart.Journal of molecular and cellular cardiology · 2013Review
- Na⁺ transport in the normal and failing heart - remember the balance.Journal of molecular and cellular cardiology · 2013Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Ca2+ transients were activated in rabbit ventricular cells by a sequence of action potential shaped voltage clamps. After activating a series of control transients, Na+ currents (INa) were inactivated with a ramp from -80 to -40 mV (1.5 s) prior to the action potential clamp. The transients were detected with the calcium indicator Fluo-4 and an epifluorescence system. With zero Na+ in the pipette INa inactivation produced a decline in the SR Ca2+ release flux (measured as the maximum rate of rise of the transient) of 27 ± 4% (n = 9, P < 0.001) and a peak amplitude reduction of 10 ± 3% (n = 9, P < 0.05). With 5 mm Na+ in the pipette the reduction in release flux was greater (34 ± 4%, n = 4, P < 0.05). The ramp effectively inactivates INa without changing ICa, and there was no significant change in the transmembrane Ca2+ flux after the inactivation of INa. We next evoked action potentials under current clamp. TTX at 100 nm, which selectively blocks neuronal isoforms of Na+ channels, produced a decline in SR Ca2+ release flux of 35 ± 3% (n = 6, P < 0.001) and transient amplitude of 12 ± 2% (n = 6, P < 0.05). This effect was similar to the effect of INa inactivation on release flux. We conclude that a TTX-sensitive INa is essential for efficient triggering of SR Ca2+ release. We propose that neuronal Na+ channels residing within couplons activate sufficient reverse Na+-Ca2+ exchanger (NCX) to prime the junctional cleft with Ca2+. The results can be explained if non-linearities in excitation-contraction coupling mechanisms modify the coupling fidelity of ICa, which is known to be low at positive potentials.
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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.