ArticleBiophysical journal2000
Block of wild-type and inactivation-deficient cardiac sodium channels IFM/QQQ stably expressed in mammalian cells.
Article in Biophysical journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Block of Voltage-Gated Sodium Channels as a Potential Novel Anti-cancer Mechanism of TIC10.Frontiers in pharmacology · 2021Article
- Anomalous enhancement of resurgent NaScientific reports · 2019Article
- The Emerging Role of Voltage-Gated Sodium Channels in Tumor Biology.Frontiers in oncology · 2019Review
- Multiple targets for flecainide action: implications for cardiac arrhythmogenesis.British journal of pharmacology · 2018Review
- Multiple modes of ryanodine receptor 2 inhibition by flecainide.Molecular pharmacology · 2014Article
- Multiple pore conformations driven by asynchronous movements of voltage sensors in a eukaryotic sodium channel.Nature communications · 2013Article
- The human Nav1.5 F1486 deletion associated with long QT syndrome leads to impaired sodium channel inactivation and reduced lidocaine sensitivity.The Journal of physiology · 2012Article
- Local anesthetic inhibition of a bacterial sodium channel.The Journal of general physiology · 2012Article
- Voltage-gated sodium channel-associated proteins and alternative mechanisms of inactivation and block.Cellular and molecular life sciences : CMLS · 2012Review
- Engineering biosynthetic excitable tissues from unexcitable cells for electrophysiological and cell therapy studies.Nature communications · 2011Article
- Molecular determinants of state-dependent block of voltage-gated sodium channels by pilsicainide.British journal of pharmacology · 2010Article
- Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmias.British journal of clinical pharmacology · 2010Review
- Drugs and Brugada syndrome patients: review of the literature, recommendations, and an up-to-date website (www.brugadadrugs.org).Heart rhythm · 2009Review
- Bupivacaine blocks N-type inactivating Kv channels in the open state: no allosteric effect on inactivation kinetics.Biophysical journal · 2008Article
- Block of persistent late Na+ currents by antidepressant sertraline and paroxetine.The Journal of membrane biology · 2008Article
- Pharmacogenetics and anti-arrhythmic drug therapy: a theoretical investigation.American journal of physiology. Heart and circulatory physiology · 2007Article
- Slow sodium channel inactivation and use-dependent block modulated by the same domain IV S6 residue.The Journal of membrane biology · 2005Article
- State-dependent block of human cardiac hNav1.5 sodium channels by propafenone.The Journal of membrane biology · 2005Article
- Block of inactivation-deficient Na+ channels by local anesthetics in stably transfected mammalian cells: evidence for drug binding along the activation pathway.The Journal of general physiology · 2004Article
- State-dependent trapping of flecainide in the cardiac sodium channel.The Journal of physiology · 2004Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of inactivation as a central mechanism in blockade of the cardiac Na(+) channel by antiarrhythmic drugs remains uncertain. We have used whole-cell and single channel recordings to examine the block of wild-type and inactivation-deficient mutant cardiac Na(+) channels, IFM/QQQ, stably expressed in HEK-293 cells. We studied the open-channel blockers disopyramide and flecainide, and the lidocaine derivative RAD-243. All three drugs blocked the wild-type Na(+) channel in a use-dependent manner. There was no use-dependent block of IFM/QQQ mutant channels with trains of 20 40-ms pulses at 150-ms interpulse intervals during disopyramide exposure. Flecainide and RAD-243 retained their use-dependent blocking action and accelerated macroscopic current relaxation. All three drugs reduced the mean open time of single channels and increased the probability of their failure to open. From the abbreviation of the mean open times, we estimated association rates of approximately 10(6)/M/s for the three drugs. Reducing the burst duration contributed to the acceleration of macroscopic current relaxation during exposure to flecainide and RAD-243. The qualitative differences in use-dependent block appear to be the result of differences in drug dissociation rate. The inactivation gate may play a trapping role during exposure to some sodium channel blocking drugs.
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