Related Concept Videos
01:18Patch Clamp
7.7K
Many fundamental cell functions such as muscle contraction and nerve transmission rely on the electrical signals produced by the movement of positively and negatively charged ions across the cell membrane. One competent method to record current flowing across the whole cell or single ion channel is the patch-clamp technique.
In this method, a glass micropipette containing electrolyte solution is tightly sealed against a small portion of the cell membrane. As a result, a patch of the cell...
In this method, a glass micropipette containing electrolyte solution is tightly sealed against a small portion of the cell membrane. As a result, a patch of the cell...
7.7K
01:30Cardiac Action Potential
11.6K
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
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
11.6K
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Related Experiment Video
Updated: Apr 21, 2026
08:11
Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
Published on: November 11, 2022
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Late cardiac sodium current can be assessed using automated patch-clamp.
Morgan Chevalier1, Bogdan Amuzescu2, Vaibhavkumar Gawali3
1Department of Clinical Research, University of Bern, Bern, 3010, Switzerland.
F1000Research
|November 11, 2014
Summary
Ranolazine reduces cardiac late sodium current, a key factor in arrhythmias. Veratridine, however, increases this current by affecting Nav1.5 channel gating.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Pharmacology
Background:
- The cardiac late sodium current (late Na+) contributes to action potential prolongation and arrhythmias.
- This current arises from voltage-dependent sodium channels (Nav1.5) entering a burst-gating mode.
- Factors like mutations, ischemia, and certain drugs can augment late Na+ current, increasing arrhythmia susceptibility.
Purpose of the Study:
- To investigate the effects of ranolazine and veratridine on cardiac late sodium current.
- To elucidate the mechanisms by which these compounds modulate Nav1.5 channel activity.
- To assess the impact of veratridine on cardiomyocyte action potential duration.
Main Methods:
- Whole-cell patch-clamp recordings in HEK293 cells expressing human Nav1.5.
- Automated patch-clamp system (CytoPatch™ 2) for precise current measurements.
- Fluctuation analysis to determine changes in channel gating parameters (open probability and number of active channels).
- Experiments in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs).
Main Results:
- Ranolazine (10 and 30 µM) significantly reduced late Na+ current.
- Veratridine (1 µM) caused a reversible increase in late Na+ current.
- Fluctuation analysis revealed ranolazine decreased mean open probability, while veratridine increased the number of active channels.
- Veratridine prolonged action potential duration in hiPSC-CMs.
- Veratridine showed minimal inhibition of hERG current at tested concentrations.
Conclusions:
- Ranolazine effectively inhibits cardiac late Na+ current, potentially through reducing channel open probability.
- Veratridine enhances late Na+ current by increasing the number of active Nav1.5 channels, likely via inactivation removal.
- These findings provide mechanistic insights into the pro-arrhythmic potential of veratridine and the anti-arrhythmic action of ranolazine.