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-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
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

1.9K
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,...
1.9K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

1.9K
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...
1.9K
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
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

1.9K
Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
1.9K
Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

1.9K
In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates,  such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow....
1.9K

You might also read

Related Articles

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

Sort by
Same author

Dental disease among adults with and without HIV in the MACS/WIHS Combined Cohort Study (MWCCS).

BMC oral health·2026
Same author

Temperature Control After In-Hospital Cardiac Arrest: Outcomes From the Discover In-Hospital Cardiac Arrest Cohort.

Critical care medicine·2026
Same author

Analysis of blood proteome in influenza-infected patients reveals new insights into the host response signatures distinguishing mild severe infections.

Frontiers in immunology·2025
Same author

The Discover In-Hospital Cardiac Arrest (Discover IHCA) Study: An Investigation of Hospital Practices After In-Hospital Cardiac Arrest.

Critical care explorations·2024
Same author

Observational study of the effect of ketamine infusions on sedation depth, inflammation, and clinical outcomes in mechanically ventilated patients with SARS-CoV-2.

Anaesthesia and intensive care·2023
Same author

Design and rationale of the CHILL phase II trial of hypothermia and neuromuscular blockade for acute respiratory distress syndrome.

Contemporary clinical trials communications·2023

Related Experiment Video

Updated: May 2, 2026

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
07:21

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

39.9K

ACE inhibitor-induced angioedema.

Michael Baram1, Anand Kommuri1, Subhashini A Sellers1

  • 1Department of Medicine, Thomas Jefferson University, Philadelphia, Pa.

The Journal of Allergy and Clinical Immunology. in Practice
|February 26, 2014
PubMed
Summary

Angiotensin-converting enzyme inhibitor (ACEI) angioedema, while often self-limiting, can necessitate airway protection. Novel treatments targeting the kallikrein-kinin system show promise for managing this condition.

Keywords:
ACEAngioedemaBradykininEcallantide

More Related Videos

Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery
09:41

Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery

Published on: December 23, 2014

16.1K
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

3.6K

Related Experiment Videos

Last Updated: May 2, 2026

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
07:21

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

39.9K
Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery
09:41

Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery

Published on: December 23, 2014

16.1K
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

3.6K

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology

Background:

  • Angiotensin-converting enzyme inhibitors (ACEI) are widely used for hypertension and kidney protection.
  • ACEI-induced angioedema is a recognized adverse effect, varying in severity from self-limiting to life-threatening airway compromise.

Observation:

  • Diagnosis of ACEI angioedema is primarily clinical, with laboratory tests used to rule out other conditions.
  • Standard treatments for allergic angioedema are ineffective for ACEI-induced cases.

Findings:

  • The pathophysiology is linked to the kallikrein-kinin system, specifically increased bradykinin levels.
  • Emerging therapies like icatibant and ecallantide, used for hereditary angioedema, have demonstrated some efficacy in ACEI-induced angioedema.

Implications:

  • Further randomized, placebo-controlled trials are essential to establish the efficacy and optimal use of icatibant and ecallantide for ACEI angioedema.
  • Understanding the kallikrein-kinin pathway is crucial for developing targeted treatments for this condition.