Jove
Visualize
Contact Us

Related Concept Videos

Regulation of Sodium and Potassium01:26

Regulation of Sodium and Potassium

1.7K
The regulation of sodium and potassium ion concentrations in the human body is a complex process governed primarily by hormones such as aldosterone, antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP).
Sodium Regulation
Sodium ions make up approximately 90% of extracellular cations, with a normal blood plasma concentration of 136–148 mEq/L. A decrease in blood volume and pressure triggers the release of renin from granular cells in the juxtaglomerular complex (JGC), primarily...
1.7K
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

1.0K
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...
1.0K
Cardiac Action Potential01:30

Cardiac Action Potential

4.9K
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
4.9K
Regulation of Heart Rates01:31

Regulation of Heart Rates

3.5K
The regulation of heart rate is a complex process controlled by the autonomic nervous system (ANS), hormonal influences, and intrinsic cardiac mechanisms. The ANS has two main components: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS).
The SNS increases heart rate through the release of norepinephrine and epinephrine, which act on beta-1 adrenergic receptors in the heart. This action increases the rate of depolarization in the sinoatrial (SA) node, the heart's...
3.5K
Electrophysiology of Normal Cardiac Rhythm01:19

Electrophysiology of Normal Cardiac Rhythm

8.4K
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...
8.4K
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

523
Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
523

You might also read

Related Articles

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

Sort by
Same author

In the era of AI, omics and organoids, animal models are still needed in cardiovascular research.

Nature reviews. Cardiology·2026
Same author

Emerging Roles for Metabolism in Myocardial Inflammation During Heart Failure.

Immunological reviews·2026
Same author

Reductive carboxylation via isocitrate dehydrogenase 1 supports cardiac metabolic adaptation during oncometabolic stress.

bioRxiv : the preprint server for biology·2026
Same author

Metabolomics-constrained modelling reveals dominant oxidative metabolism in the Egyptian fruit bat myocardium.

PloS one·2026
Same author

The isolated working guinea pig heart: A functional and electrophysiological characterisation.

Experimental physiology·2026
Same author

Investigating short-term lung inflammation using exhaled breath VOCs from exposure to candles: a randomized controlled crossover study among young mild asthmatics.

Journal of breath research·2026
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 Experiment Video

Updated: Dec 10, 2025

Camera-based Measurements of Intracellular [Na+] in Murine Atrial Myocytes
10:08

Camera-based Measurements of Intracellular [Na+] in Murine Atrial Myocytes

Published on: May 27, 2022

1.4K

Intracellular sodium elevation reprograms cardiac metabolism.

Dunja Aksentijević1,2, Anja Karlstaedt3, Marina V Basalay1

  • 1School of Cardiovascular and Medical Sciences, British Heart Foundation Centre of Research Excellence, King's College London, The Rayne Institute, St Thomas' Hospital, London, UK.

Nature Communications
|August 30, 2020
PubMed
Summary

Elevated intracellular sodium (Na) in the heart triggers metabolic changes, shifting energy use from fats to carbohydrates. Targeting sodium or mitochondrial exchangers may treat heart failure metabolic issues.

More Related Videos

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
11:00

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

10.5K
Isolation of Atrial Cardiomyocytes from a Rat Model of Metabolic Syndrome-related Heart Failure with Preserved Ejection Fraction
08:31

Isolation of Atrial Cardiomyocytes from a Rat Model of Metabolic Syndrome-related Heart Failure with Preserved Ejection Fraction

Published on: July 26, 2018

10.6K

Related Experiment Videos

Last Updated: Dec 10, 2025

Camera-based Measurements of Intracellular [Na+] in Murine Atrial Myocytes
10:08

Camera-based Measurements of Intracellular [Na+] in Murine Atrial Myocytes

Published on: May 27, 2022

1.4K
Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
11:00

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

10.5K
Isolation of Atrial Cardiomyocytes from a Rat Model of Metabolic Syndrome-related Heart Failure with Preserved Ejection Fraction
08:31

Isolation of Atrial Cardiomyocytes from a Rat Model of Metabolic Syndrome-related Heart Failure with Preserved Ejection Fraction

Published on: July 26, 2018

10.6K

Area of Science:

  • Cardiovascular Physiology
  • Cardiac Metabolism
  • Molecular Cardiology

Background:

  • Intracellular sodium (Na) elevation is a key feature of heart pathologies involving metabolic remodeling.
  • Understanding the link between Na and metabolic changes is crucial for treating heart failure.

Purpose of the Study:

  • To investigate if acute or chronic intracellular Na overload causally links to cardiac metabolic remodeling.
  • To identify a common Na-mediated metabolic signature in the failing heart.

Main Methods:

  • Utilized Langendorff-perfused mouse hearts (control, transgenic, ouabain-treated, hypertrophied).
  • Employed multi-nuclear magnetic resonance spectroscopy (23Na, 31P, 13C NMR) and 1H-NMR metabolomic profiling.
  • Performed in silico modeling of metabolic fluxes.

Main Results:

  • Elevated intracellular Na induced adaptive metabolic alterations, including a shift from fatty acid to carbohydrate metabolism.
  • Observed changes in glycolytic, anaplerotic, and Krebs cycle intermediate concentrations.
  • Inhibition of the mitochondrial Na/Ca exchanger ameliorated these metabolic changes.
  • In silico modeling revealed altered metabolic fluxes across multiple pathways.

Conclusions:

  • Acute and chronic Na overload are causally linked to cardiac metabolic remodeling.
  • A common Na-mediated metabolic fingerprint exists in the failing heart.
  • Targeting Na overload or mitochondrial Na/Ca exchange may offer novel therapeutic strategies for heart failure.