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

2.2K
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...
2.2K
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

1.2K
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,...
1.2K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

867
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...
867
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

2.3K
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...
2.3K
Cardiac Catheterization IV: Nursing Management01:26

Cardiac Catheterization IV: Nursing Management

592
Nursing responsibilities before cardiac catheterization include:Assess for allergies and establish baseline health status.Before cardiac catheterization, assess the patient for allergies to contrast dye. Perform a comprehensive baseline assessment, including vital signs, heart and breath sounds, and a neurovascular assessment of the extremities, noting distal pulses, skin color, and temperature. Instruct the patient to fast for 8-12 hours before the procedure. Evaluate baseline laboratory...
592
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

405
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...
405

You might also read

Related Articles

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

Sort by
Same author

Clinical experience with berotralstat in patients with hereditary angioedema: an Italian case series from the ITACA cohort.

European annals of allergy and clinical immunology·2026
Same author

Rare connective tissue diseases in patients with C1-inhibitor deficiency hereditary angioedema: first evidence on prevalence and distribution from a large Italian cohort study.

Frontiers in immunology·2024
Same author

Vertical heterostructure of graphite-MoS<sub>2</sub> for gas sensing.

Nanoscale horizons·2024
Same author

Search for New Phenomena in Two-Body Invariant Mass Distributions Using Unsupervised Machine Learning for Anomaly Detection at sqrt[s]=13  TeV with the ATLAS Detector.

Physical review letters·2024
Same author

Contact System Activation and Bradykinin Generation in Patients With Idiopathic Angioedema.

Journal of investigational allergology & clinical immunology·2024
Same author

Evidence for the Higgs Boson Decay to a Z Boson and a Photon at the LHC.

Physical review letters·2024
Same journal

Safety, Adherence, and Effectiveness of an Increased Dose of Pollinex Quattro Grass and/or Olive in Real-World Practice.

Journal of investigational allergology & clinical immunology·2026
Same journal

Effect of Dupilumab on Sleep Disturbance in Patients With Uncontrolled Moderate-to-Severe Asthma, Type 2 Inflammation, and Nocturnal Awakenings: The MORPHEO Randomized Controlled Trial.

Journal of investigational allergology & clinical immunology·2026
Same journal

Severe Rituximab-Induced Cytokine Release Syndrome After Desensitization Successfully Treated With Tocilizumab: A Case Report.

Journal of investigational allergology & clinical immunology·2026
Same journal

Dysregulation of Mast Cell Prostaglandin in Food Anaphylaxis.

Journal of investigational allergology & clinical immunology·2026
Same journal

Extract-Negative Cofactor-Dependent Shrimp Anaphylaxis Caused by IgE Reactivity to Insoluble Muscle Proteins.

Journal of investigational allergology & clinical immunology·2026
Same journal

Antibiotic Allergy Labels in Hospitalized Patients: Results of a Multicenter Cross-Sectional Study.

Journal of investigational allergology & clinical immunology·2026
See all related articles

Related Experiment Video

Updated: Jan 6, 2026

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

3.9K

Angiotensin-Converting Enzyme Inhibitor-Associated Angioedema: From Bed to Bench.

L Carucci1, M Bova2, A Petraroli2

  • 1Post-Graduate Program in Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy.

Journal of Investigational Allergology & Clinical Immunology
|October 11, 2019
PubMed
Summary
This summary is machine-generated.

Angiotensin-converting enzyme inhibitor-associated angioedema (ACEI-AAE) involves higher levels of VEGF-A, VEGF-C, and sPLA2, suggesting their role in pathogenesis. Sartans are a safe alternative for patients with ACEI-AAE.

Keywords:
AngioedemaAngiotensin-converting enzyme inhibitorBiomarkersC1-inhibitorGenetic analysisPhospholipases A2Vascular endothelial growth factor AVascular endothelial growth factor C

More Related Videos

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

39.0K
Improved Home Blood Pressure Control by CT-guided Ozone-mediated Renal Denervation for Patients with Resistant Hypertension
04:37

Improved Home Blood Pressure Control by CT-guided Ozone-mediated Renal Denervation for Patients with Resistant Hypertension

Published on: June 6, 2025

615

Related Experiment Videos

Last Updated: Jan 6, 2026

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

3.9K
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

39.0K
Improved Home Blood Pressure Control by CT-guided Ozone-mediated Renal Denervation for Patients with Resistant Hypertension
04:37

Improved Home Blood Pressure Control by CT-guided Ozone-mediated Renal Denervation for Patients with Resistant Hypertension

Published on: June 6, 2025

615

Area of Science:

  • Immunology
  • Pharmacology
  • Vascular Biology

Background:

  • Angiotensin-converting enzyme inhibitor-associated angioedema (ACEI-AAE) affects 0.1%-0.7% of patients on ACE inhibitors.
  • The exact pathogenesis of ACEI-AAE, particularly the role of vascular permeability, remains unclear.

Purpose of the Study:

  • To characterize clinical, genetic, and laboratory features of ACEI-AAE.
  • To explore the involvement of VEGF-A, VEGF-C, Ang1/Ang2, and sPLA2 in ACEI-AAE pathogenesis.

Main Methods:

  • Collected clinical and laboratory data from 51 ACEI-AAE patients and controls.
  • Performed genetic analysis for SERPING1, ANGPT1, PLG, and F12 mutations.
  • Measured plasma levels of VEGF-A, VEGF-C, Ang1/Ang2, and sPLA2.

Main Results:

  • The average onset of ACEI-AAE was 3 years after starting ACEI therapy.
  • Elevated plasma levels of VEGF-A, VEGF-C, and sPLA2 were observed in ACEI-AAE patients compared to controls.
  • No significant mutations were found in the analyzed genes, and Ang1/Ang2 levels were unchanged.

Conclusions:

  • Switching to sartans appears safe for patients with a history of ACEI-AAE.
  • Increased VEGF-A, VEGF-C, and sPLA2 suggest a role in the pathophysiology of ACEI-AAE.