ArticleBritish journal of pharmacology2010
Riluzole protects against cardiac ischaemia and reperfusion damage via block of the persistent sodium current.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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16 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- A systematic review and functionalFrontiers in neuroscience · 2025Pooled it
- Riluzole is associated with reduced risk of heart failure.European journal of neurology · 2025Article
- Interrelated In Vitro Mechanisms of Sibutramine-Induced Cardiotoxicity.Cardiovascular toxicology · 2021Article
- Tetrodotoxin-Sensitive Neuronal-Type NaJournal of the American Heart Association · 2020Article
- Tandem pore TWIK-related potassium channels and neuroprotection.Neural regeneration research · 2019Review
- Ischemia-reperfusion injury: evidences for translational research.Annals of translational medicine · 2016Article
- Neuronal Na+ channel blockade suppresses arrhythmogenic diastolic Ca2+ release.Cardiovascular research · 2015Article
- Partial block by riluzole of muscle sodium channels in myotubes from amyotrophic lateral sclerosis patients.Neurology research international · 2014Article
- The role of late I Na in development of cardiac arrhythmias.Handbook of experimental pharmacology · 2014Review
- Coupled left-shift of Nav channels: modeling the Na⁺-loading and dysfunctional excitability of damaged axons.Journal of computational neuroscience · 2012Article
- Neurological perspectives on voltage-gated sodium channels.Brain : a journal of neurology · 2012Review
- Left-shifted nav channels in injured bilayer: primary targets for neuroprotective nav antagonists?Frontiers in pharmacology · 2012Article
- Regulation and function of the two-pore-domain (K2P) potassium channel Trek-1 in alveolar epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Inhibition of Navβ4 peptide-mediated resurgent sodium currents in Nav1.7 channels by carbamazepine, riluzole, and anandamide.Molecular pharmacology · 2011Article
- Recent developments regarding voltage-gated sodium channel blockers for the treatment of inherited and acquired neuropathic pain syndromes.Frontiers in pharmacology · 2011Article
- The persistent sodium current blocker riluzole is antiarrhythmic and anti-ischaemic in a pig model of acute myocardial infarction.PloS one · 2010Article
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeCurrent strategies to ameliorate cardiac ischaemic and reperfusion damage, including block of the sodium-hydrogen exchanger, are therapeutically ineffective. Here we propose a different approach, block of the persistent sodium current (INaP). EXPERIMENTAL APPROACH: Left ventricular pressure was measured as an index of functional deficit in isolated, Langendorff perfused, hearts from adult rats, subjected to 30 min global ischaemia and reperfusion with vehicle only (control) or riluzole (1-10 microM) in the perfusate. Cell shortening and intracellular Ca2+ concentrations [Ca2+](i) were measured in adult rat isolated myocytes subjected to hypoxia and re-oxygenation. The block of transient and persistent sodium currents by concentrations of riluzole between 0.01 and 100 microM were assessed in rat isolated myocytes using patch clamp techniques. KEY
resultsIn perfused hearts, riluzole produced a concentration-dependent cardioprotective action, with minor protection from 1 microM and produced rapid and almost complete recovery upon reperfusion from 3 and 10 microM. In isolated myocytes, riluzole at 3 and 10 microM greatly attenuated or prevented the hypoxia- and reperfusion-induced rise in [Ca2+](i) and the contractile deficit. In patch clamp experiments, riluzole blocked the persistent sodium current with an IC(50) of 2.7 microM, whereas the block of the transient sodium current was only apparent at concentrations above 30 microM. CONCLUSIONS AND IMPLICATIONS: Riluzole preferentially blocked INaP and was protective in cardiac ischaemia and reperfusion. Thus block of the persistent sodium current would be a viable method of ameliorating cardiac ischaemic and reperfusion damage.
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