Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...

Mechanism of Cardiac Arrhythmias

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.

Voltage-gated Ion Channels

Voltage-gated Ion Channels

Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.
Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of...

Voltage-gated Ion Channels

Voltage-gated Ion Channels

Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.
Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of...

Cardiomyopathy I: Introduction and Classification

Cardiomyopathy I: Introduction and Classification

Cardiomyopathy, or CMP, is a group of diseases affecting the myocardial structure, impairing its ability to pump blood effectively. This condition can lead to arrhythmias, heart failure, or sudden cardiac death.Cardiomyopathies are classified into primary and secondary categories:Primary Cardiomyopathy refers to conditions involving only the heart muscle that are often idiopathic (of unknown cause) or genetic. They primarily affect the myocardium without the involvement of other systemic...

Cardiac Action Potential

Cardiac Action Potential

Cardiac action potentials are essential for proper heart function, enabling the rhythmic contractions needed for adequate blood circulation. Nodal cells and Purkinje fibers, specialized for electrical conduction, generate these action potentials.
The cardiac action potential process involves a series of phases characterized by the movement of ions across the cardiac cell membranes, leading to the depolarization and repolarization of the cardiac myocytes.
Ionic Basis of Cardiac Action Potentials

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Perspectives on phenotype in genetic testing for early-onset atrial fibrillation.

European journal of human genetics : EJHG·2026

Same author

AAV-mediated long-term TBX18 expression causes cardiac fibrosis and fails to induce pacemaker activity in rodents.

The Journal of clinical investigation·2026

Same author

Artificial intelligence-enhanced wearable technology enables ventricular arrhythmia prediction.

European heart journal. Digital health·2026

Same author

Impact of extended rhythm monitoring on arrhythmic risk estimates in phospholamban cardiomyopathy.

Heart rhythm·2026

Same author

Laminopathies: natural history and risk prediction of heart failure.

European heart journal·2026

Same author

Effect of a grace period on false alarm rates of smartwatch-based out-of-hospital cardiac arrest detection systems: a pilot study.

Resuscitation plus·2026

Search research articles

Related Experiment Video

Updated: Jun 16, 2026

Dual-Dye Optical Mapping of Hearts from RyR2R2474S Knock-In Mice of Catecholaminergic Polymorphic Ventricular Tachycardia

Dual-Dye Optical Mapping of Hearts from RyR2^R2474S Knock-In Mice of Catecholaminergic Polymorphic Ventricular Tachycardia

Published on: December 22, 2023

Cardiac sodium channelopathies.

Ahmad S Amin¹, Alaleh Asghari-Roodsari, Hanno L Tan

¹Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.

Pflugers Archiv : European Journal of Physiology

|January 22, 2010

Summary

This summary is machine-generated.

Cardiac sodium channelopathies, caused by mutations in SCN5A and other genes, lead to arrhythmias. Understanding these channelopathies is key to developing targeted therapies for conditions like long QT and Brugada syndrome.

More Related Videos

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique

Published on: November 11, 2022

Determination of the Relative Cell Surface and Total Expression of Recombinant Ion Channels Using Flow Cytometry

Determination of the Relative Cell Surface and Total Expression of Recombinant Ion Channels Using Flow Cytometry

Published on: September 28, 2016

Related Experiment Videos

Last Updated: Jun 16, 2026

Dual-Dye Optical Mapping of Hearts from RyR2R2474S Knock-In Mice of Catecholaminergic Polymorphic Ventricular Tachycardia

Dual-Dye Optical Mapping of Hearts from RyR2^R2474S Knock-In Mice of Catecholaminergic Polymorphic Ventricular Tachycardia

Published on: December 22, 2023

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique

Published on: November 11, 2022

Determination of the Relative Cell Surface and Total Expression of Recombinant Ion Channels Using Flow Cytometry

Determination of the Relative Cell Surface and Total Expression of Recombinant Ion Channels Using Flow Cytometry

Published on: September 28, 2016

Area of Science:

Cardiovascular Physiology
Molecular Cardiology
Genetics of Cardiac Diseases

Background:

Cardiac sodium channels (INa) are crucial for cardiomyocyte electrical activity.
Mutations in cardiac sodium channel genes cause channelopathies, leading to arrhythmias.
SCN5A gene mutations are a primary cause of inherited cardiac arrhythmias.

Purpose of the Study:

To review the structure, function, and genetics of cardiac sodium channels.
To summarize the molecular mechanisms underlying cardiac sodium channelopathies.
To discuss recent advances in mutation-specific therapies for these channelopathies.

Main Methods:

Review of clinical and genetic studies.
Analysis of biophysical studies in heterologous expression systems and mouse models.
Synthesis of current knowledge on cardiac sodium channelopathies.

Main Results:

Mutations increasing INa cause long QT syndrome.
Mutations decreasing INa induce Brugada syndrome, progressive cardiac conduction disease, and sick sinus syndrome.
Cardiac sodium channel dysfunction is linked to dilated cardiomyopathy, atrial fibrillation, and SIDS.

Conclusions:

Cardiac sodium channelopathies encompass a spectrum of arrhythmogenic diseases.
Understanding genotype-phenotype correlations is vital for diagnosis and management.
Mutation-specific therapies offer a promising future for treating these channelopathies.