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

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

413
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
413
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

578
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
578
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

332
β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
332
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

674
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
674
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

355
Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
355
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

521
The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
521

You might also read

Related Articles

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

Sort by
Same author

Atherosclerosis Progression Evaluation in Coronary Arteries by Computed Tomography Compared to Peripheral Vessels Using 3D Ultrasonography.

Journal of clinical medicine·2026
Same author

Coronary Culprit Lesion Location and Intramyocardial Hemorrhage in STEMI.

Circulation. Cardiovascular imaging·2026
Same author

Cardiac autonomic function in elderly patients with and without atrial fibrillation.

European heart journal open·2026
Same author

Higher Daily Temperature Is Associated With Prolonged Device-Detected Atrial Fibrillation Episodes.

Circulation. Arrhythmia and electrophysiology·2025
Same author

AI-ECG-derived biological age as a predictor of mortality in cardiovascular and acute care patients.

European heart journal. Digital health·2025
Same author

Pulmonary Vein Isolation Only for Atrial Fibrillation With Heart Failure (POLAR-HF).

JACC. Clinical electrophysiology·2025

Related Experiment Video

Updated: Jun 18, 2025

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

3.1K

Angiotensin Receptor-Neprilysin Inhibitor Is Associated With Improved Cardiac Autonomic Function in Heart Failure.

Andreas A Boehmer1, Tim Schubert1, Moritz Rothe1

  • 1Division of Cardiology St. Josefs-Hospital Wiesbaden Wiesbaden Germany.

Journal of the American Heart Association
|July 31, 2024
PubMed
Summary

Sacubitril/valsartan (ARNI) therapy significantly improved cardiac autonomic function in patients with heart failure with reduced ejection fraction. This enhancement in parasympathetic tone may be linked to the drug's volume-unloading effects.

Keywords:
ARNIcardiac autonomic nervous systemheart failureheart rate variabilityparasympathetic

More Related Videos

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
07:24

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

Published on: April 8, 2013

24.2K
A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

4.7K

Related Experiment Videos

Last Updated: Jun 18, 2025

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

3.1K
Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
07:24

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

Published on: April 8, 2013

24.2K
A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

4.7K

Area of Science:

  • Cardiology
  • Autonomic Nervous System Research
  • Pharmacology

Background:

  • Heart failure with reduced ejection fraction (HFrEF) is linked to autonomic nervous system imbalance.
  • Sacubitril/valsartan (ARNI) is known to reduce mortality and hospitalizations in HFrEF.
  • The impact of ARNI on the cardiac autonomic nervous system remains understudied.

Purpose of the Study:

  • To investigate the effects of ARNI therapy on the cardiac autonomic nervous system in HFrEF patients.
  • To assess changes in heart rate variability, heart rate, deceleration capacity, and repolarization dynamics.
  • To correlate autonomic changes with ventricular function and NT-proBNP levels.

Main Methods:

  • Prospective, single-center cohort study involving 63 HFrEF patients.
  • Standardized 12-lead Holter-ECG, echocardiography, and laboratory tests before and 3 months after ARNI initiation.
  • Analysis of heart rate variability (SDNN, RMSSD), heart rate, deceleration capacity, and periodic repolarization dynamics.

Main Results:

  • ARNI therapy significantly increased heart rate variability (SDNN: 25 to 36 ms, P<0.001; RMSSD: 12 to 19 ms, P<0.001).
  • Heart rate decreased (73±9 to 67±4 bpm, P<0.001), and deceleration capacity improved (2.1 to 4.4 ms, P<0.001).
  • Improvements in autonomic function correlated with enhanced left ventricular ejection fraction (29±6% to 40±8%, P<0.001) and reduced NT-proBNP (P<0.001).

Conclusions:

  • Three months of ARNI therapy significantly increased cardiac parasympathetic tone in HFrEF patients.
  • Autonomic improvement may be mediated by volume unloading, contributing to ARNI's benefits.
  • ARNI therapy positively modulates the cardiac autonomic nervous system in HFrEF.