Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

1.1K
Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
1.1K
Antiepileptic Drugs: Potassium Channel Activators01:20

Antiepileptic Drugs: Potassium Channel Activators

232
Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
Ezogabine has gained approval as an adjunctive treatment...
232
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

1.5K
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,...
1.5K
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

659
Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
659
Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

999
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.
999

You might also read

Related Articles

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

Sort by
Same author

Publication fraud in the era of generative artificial intelligence.

British journal of pharmacology·2026
Same author

Propafenone-mediated gap junctional uncoupling results from aberrant connexin-43 trafficking.

Pharmacological reports : PR·2026
Same author

Opening closed inward rectifier potassium channel doors.

British journal of pharmacology·2026
Same author

Intoxication by Self-administered Cesium Salts, the Clinical Impact of Questionable Research Output.

Cardiovascular toxicology·2026
Same author

Exploring the Cell Biological and Functional Effects of the First Disease Associated KCC1 Genetic Variant.

Journal of cellular physiology·2025
Same author

Arrhythmia Inducibility in the CAVB Dog Model, A Critical Analysis on Underlying Factors.

Cardiovascular toxicology·2025

Related Experiment Video

Updated: Aug 5, 2025

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes
11:33

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes

Published on: March 12, 2013

13.5K

Chronic Propafenone Application Increases Functional KIR2.1 Expression In Vitro.

Encan Li1, Willy Kool1, Liset Woolschot1

  • 1Department of Medical Physiology, Division of Heart & Lungs, University Medical Center Utrecht, Yalelaan 50, 3584 CM Utrecht, The Netherlands.

Pharmaceuticals (Basel, Switzerland)
|March 29, 2023
PubMed
Summary

Propafenone, an antiarrhythmic drug, acts as an agonist for inwardly rectifying potassium (KIR)2.1 channels. Chronic exposure to propafenone increases KIR2.1 expression and function, potentially by inhibiting pre-lysosomal trafficking.

Keywords:
AgoKirKIR2.1long-term effectspropafenonetrafficking

More Related Videos

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
08:11

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

Published on: November 11, 2022

2.9K
High-Throughput Optical Controlling and Recording Calcium Signal in iPSC-Derived Cardiomyocytes for Toxicity Testing and Phenotypic Drug Screening
10:01

High-Throughput Optical Controlling and Recording Calcium Signal in iPSC-Derived Cardiomyocytes for Toxicity Testing and Phenotypic Drug Screening

Published on: March 31, 2022

3.2K

Related Experiment Videos

Last Updated: Aug 5, 2025

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes
11:33

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes

Published on: March 12, 2013

13.5K
Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
08:11

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

Published on: November 11, 2022

2.9K
High-Throughput Optical Controlling and Recording Calcium Signal in iPSC-Derived Cardiomyocytes for Toxicity Testing and Phenotypic Drug Screening
10:01

High-Throughput Optical Controlling and Recording Calcium Signal in iPSC-Derived Cardiomyocytes for Toxicity Testing and Phenotypic Drug Screening

Published on: March 31, 2022

3.2K

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Ion Channel Function

Background:

  • Inwardly rectifying potassium (KIR) channels, particularly KIR2.1, are crucial for cardiac action potential regulation and membrane stability.
  • Dysfunctional KIR2.1 channels are implicated in Andersen-Tawil Syndrome (ATS) and heart failure.
  • Agonists of KIR2.1 (AgoKirs) represent a potential therapeutic strategy for restoring channel function.

Purpose of the Study:

  • To investigate the long-term effects of propafenone, a known AgoKir, on KIR2.1 protein expression, subcellular localization, and function in vitro.
  • To elucidate the underlying mechanisms of propafenone's chronic effects on KIR2.1.

Main Methods:

  • Single-cell patch-clamp electrophysiology to measure KIR2.1 currents.
  • Western blot analysis to quantify KIR2.1 protein expression levels.
  • Conventional immunofluorescence and live-imaging microscopy to assess subcellular localization of KIR2.1 proteins.

Main Results:

  • Acute, low-concentration propafenone treatment confirmed its AgoKir activity without affecting KIR2.1 protein handling.
  • Chronic propafenone treatment (at significantly higher concentrations) led to increased KIR2.1 protein expression and current densities.
  • These chronic effects may be linked to the inhibition of pre-lysosomal trafficking pathways.

Conclusions:

  • Propafenone exhibits dual effects on KIR2.1 channels: acute agonism and chronic upregulation of expression and function.
  • The chronic upregulation of KIR2.1 by propafenone is potentially mediated by interference with pre-lysosomal trafficking.
  • These findings provide insights into the long-term molecular mechanisms of propafenone action on cardiac ion channels.