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Related Concept Videos

Electrophysiology of Normal Cardiac Rhythm01:19

Electrophysiology of Normal Cardiac Rhythm

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The normal cardiac rhythm is a synchronized electrical activity that facilitates the regular and coordinated contraction of the heart muscle. This process is essential for efficient blood circulation throughout the body. The fundamental elements involved in establishing and maintaining this rhythm include the unique electrical properties of cardiac muscle cells, the sinoatrial (SA) node's pacemaker function, the specialized conducting system, and the ionic mechanisms underlying each phase...
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Conduction System of the Heart01:19

Conduction System of the Heart

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Autorhythmicity is a term that refers to the heart's inherent ability to generate electrical signals and instigate muscle contractions. This self-regulating conduction system within the heart consists of two key components: the pacemaker cells and specialized conducting cells.
The pacemaker cells are located in two primary nodes: the sinoatrial (SA) node and the atrioventricular (AV) node. The SA node pacemaker cells can autonomously depolarize, triggering an action potential that leads to the...
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Conduction System of the Heart01:20

Conduction System of the Heart

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The cardiac conduction system produces and transmits electrical impulses that prompt myocardial contraction, ensuring efficient heart function. This intricate system ensures that the heart beats in a coordinated and efficient manner, beginning with the atria and then the ventricles. The conduction system optimizes cardiac output by maintaining this precise sequence, which is crucial for adequate blood circulation.
This system relies on the unique properties of nodal and Purkinje cells:...
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Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

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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.
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Cardiac Action Potential01:30

Cardiac Action Potential

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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
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Smooth Muscle Contraction01:25

Smooth Muscle Contraction

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Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
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Related Experiment Video

Updated: Mar 1, 2026

Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling
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Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling

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TNFα Modulates Cardiac Conduction by Altering Electrical Coupling between Myocytes.

Sharon A George1, Patrick J Calhoun2, Robert G Gourdie1,3

  • 1Department of Biomedical Engineering and Sciences, Virginia Polytechnic Institute and State UniversityBlacksburg, VA, United States.

Frontiers in Physiology
|June 8, 2017
PubMed
Summary

Elevating extracellular calcium during acute Tumor Necrosis Factor α (TNFα) exposure improves cardiac electrical coupling and conduction velocity (CV). This approach may prevent inflammation-induced CV slowing.

Keywords:
TNFαcalciumconductionconnexin43ephaptic coupling

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Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes

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Area of Science:

  • Cardiovascular Physiology
  • Cardiac Electrophysiology
  • Inflammation Biology

Background:

  • Tumor Necrosis Factor α (TNFα) is upregulated during acute inflammation, affecting cardiac function.
  • TNFα may alter cardiac gap junctional (GJ) coupling and ephaptic coupling by modulating Connexin43 and vascular permeability.
  • This study investigates TNFα's impact on cardiac electrical coupling and conduction velocity (CV).

Purpose of the Study:

  • To test the hypothesis that acute pathophysiological TNFα levels modulate cardiac CV by altering GJ and ephaptic coupling.
  • To investigate the effects of elevated extracellular calcium on TNFα-induced changes in cardiac electrical properties.
  • To explore a potential therapeutic strategy for inflammation-induced cardiac conduction slowing.

Main Methods:

  • Optical mapping of guinea pig hearts to measure CV (longitudinal and transverse) under control, TNFα, and TNFα + high calcium conditions.
  • Transmission electron microscopy to quantify changes in the extracellular nanodomain-perinexus (Wp) adjacent to gap junctions.
  • Western blotting for Cx43 expression/phosphorylation and confocal immunofluorescence for Cx43 distribution.

Main Results:

  • TNFα alone slowed transverse CV (CVt) and increased Wp, indicating altered electrical coupling.
  • Increasing extracellular calcium during TNFα exposure rapidly restored CVt and reduced Wp to control levels.
  • Combined TNFα and high calcium treatment also improved GJ coupling, contributing to enhanced CV.

Conclusions:

  • Elevating extracellular calcium during acute TNFα exposure mitigates perinexal expansion.
  • This intervention enhances both ephaptic and GJ coupling, leading to improved cardiac CV.
  • High extracellular calcium may represent a novel strategy to prevent inflammation-induced cardiac conduction slowing.