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

Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

2.9K
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...
2.9K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

1.3K
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...
1.3K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

2.7K
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...
2.7K
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

525
Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
525
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

1.7K
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,...
1.7K
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

453
Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
453

You might also read

Related Articles

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

Sort by
Same author

Hafnium-Substituted Wells-Dawson Polyoxometalate as a High-Performance Contrast Agent for Transmission Electron Microscopy of Biological Ultrastructure.

International journal of molecular sciences·2026
Same author

Non-Destructive Characterization of Cultural Heritage Materials Using a Modified Acoustic Resonance Approach.

Materials (Basel, Switzerland)·2026
Same author

Injury Epidemiology in Elite U17 Football Players: A Prospective Study Across Six Competitive Seasons.

Life (Basel, Switzerland)·2026
Same author

Linking satellite-derived vegetation health parameters to arborist ground observations in urban environment.

Scientific reports·2026
Same author

Pathological and Diagnostic Assessment of Duodenal Wound Healing: A Comparative Experimental Study of Jejunal Serosal vs. ePTFE Patch Repair.

Medicina (Kaunas, Lithuania)·2026
Same author

Lycopene Mitigates Rat Liver Damage Induced by Lipopolysaccharide via Mechanisms Involving Oxidative Stress, Inflammation, and Apoptosis.

Current issues in molecular biology·2025

Related Experiment Video

Updated: Mar 10, 2026

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
07:46

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

Published on: October 15, 2010

44.6K

Angiotensin receptor blockers & endothelial dysfunction: Possible correlation & therapeutic implications.

Miroslav Radenkovic1, Marko Stojanović1, Ivana Milićević Nešić1

  • 1Department of Pharmacology, Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.

The Indian Journal of Medical Research
|December 10, 2016
PubMed
Summary

Angiotensin receptor blockers can improve endothelial dysfunction (ED), a key factor in atherosclerosis development. This review examines clinical studies on their therapeutic benefits and broader effects on vascular health.

More Related Videos

Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
08:42

Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research

Published on: October 22, 2014

28.1K
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

5.7K

Related Experiment Videos

Last Updated: Mar 10, 2026

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
07:46

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

Published on: October 15, 2010

44.6K
Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
08:42

Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research

Published on: October 22, 2014

28.1K
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

5.7K

Area of Science:

  • Cardiovascular Medicine
  • Endothelial Biology
  • Pharmacology

Background:

  • Endothelial dysfunction (ED) disrupts vascular homeostasis, contributing to atherosclerosis.
  • Imbalance in nitric oxide and angiotensin II (Ang II) production is a critical factor in ED.
  • ED is an early stage of atherosclerosis and may be reversible.

Purpose of the Study:

  • To review clinical studies on angiotensin receptor blockers (ARBs) for improving ED.
  • To explore the pleiotropic effects of ARBs related to ED improvement.
  • To summarize current therapeutic strategies for ED.

Main Methods:

  • Systematic review of prospective, randomized, double-blind, placebo or active-controlled clinical trials.
  • Focus on studies investigating ARBs and their impact on endothelial function.
  • Evaluation of evidence regarding the role of Ang II in ED.

Main Results:

  • ARBs have demonstrated effectiveness in improving ED.
  • Pleiotropic actions of ARBs contribute to enhanced endothelial function.
  • Clinical evidence supports ARBs as a therapeutic option for ED.

Conclusions:

  • ARBs represent a promising therapeutic strategy for managing endothelial dysfunction.
  • Targeting the renin-angiotensin system with ARBs can ameliorate ED and potentially atherosclerosis.
  • Further research into ARBs' multifaceted benefits is warranted.