ArticlePflugers Archiv : European journal of physiology2007
Downregulation of neuronal sodium channel subunits Nav1.1 and Nav1.6 in the sinoatrial node from volume-overloaded heart failure rat.
Article in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 42 citations in OpenAlex.
- Distribution of Voltage-Gated Sodium Channels and Scaffolding Proteins on Vestibular Calyx Ending Delineates the Axon Initial Segment.The Journal of comparative neurology · 2026Article
- Heart failure in mice induces a dysfunction of the sinus node associated with reduced CaMKII signaling.The Journal of general physiology · 2022Article
- Neuregulin-1β Partially Improves Cardiac Function in Volume-Overload Heart Failure Through Regulation of Abnormal Calcium Handling.Frontiers in pharmacology · 2019Article
- Differential Expression of Ion Channels in Adult and Neonatal Rat Ventral Respiratory Column.Journal of molecular neuroscience : MN · 2018Article
- β1-Adrenergic blocker bisoprolol reverses down-regulated ion channels in sinoatrial node of heart failure rats.Journal of physiology and biochemistry · 2016Article
- Apamin-Sensitive K+ Current Upregulation in Volume-Overload Heart Failure is Associated with the Decreased Interaction of CK2 with SK2.The Journal of membrane biology · 2015Article
- The genetic basis for inherited forms of sinoatrial dysfunction and atrioventricular node dysfunction.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2015Review
- Ca(2+) cycling properties are conserved despite bradycardic effects of heart failure in sinoatrial node cells.Frontiers in physiology · 2015Article
- Genomic biomarkers of SUDEP in brain and heart.Epilepsy & behavior : E&B · 2014Review
- Post-translational modifications of the cardiac Na channel: contribution of CaMKII-dependent phosphorylation to acquired arrhythmias.American journal of physiology. Heart and circulatory physiology · 2013Review
- Rbfox proteins regulate alternative splicing of neuronal sodium channel SCN8A.Molecular and cellular neurosciences · 2012Article
- A null mutation of the neuronal sodium channel NaV1.6 disrupts action potential propagation and excitation-contraction coupling in the mouse heart.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Loss of cerebrovascular Shaker-type K(+) channels: a shared vasodilator defect of genetic and renal hypertensive rats.American journal of physiology. Heart and circulatory physiology · 2009Article
- Is sodium current present in human sinoatrial node cells?International journal of biological sciences · 2009Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium current I(Na) plays an important role in the pacemaker activity of the sinoatrial node (SAN). However, expression profiles of corresponding sodium channel subunits in normal SAN remain unclear. And little is known about expression alteration of sodium channel in SAN under heart failure (HF) condition. We assessed SAN function and expression of Nav1.1, Nav1.2, Nav1.3, Nav1.5, Nav1.6, and Nav1.7 in sham-operated rats and rats subjected to abdominal arteriovenous shunt (volume overload)-induced HF. Immunohistochemistry, Western blot, and quantitative real-time reverse transcriptase PCR analysis were used to quantify sodium channel subunit protein and mRNA expression in the SAN. Intrinsic heart rate declined and sinus node recovery time was prolonged in HF rats, indicating suppressed SAN pacemaker function. In rat SAN, Nav1.1 and Nav1.6 were the primary subunits, Nav1.5 and Nav1.7 were weakly expressed, and Nav1.2 and Nav1.3 were not found to be present. HF significantly decreased SAN sodium channel expression at both the protein and mRNA levels (Nav1.1 by 61 and 71%, Nav1.6 by 49 and 46%, respectively). In conclusion, Nav1.1 and Nav1.6 are the dominant subunits in rat SAN, and downregulation of Nav1.1 and Nav1.6 expression contributes to HF-induced SAN dysfunction. These findings provide additional information about molecular basis of disease-related impairment of SAN function.
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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.