Related Experiment Video
Updated: May 2, 2026
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
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.
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.
Related Concept Videos
01:30Antihypertensive 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
01:25Antihypertensive 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
01:26Heart 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
01:30Antihypertensive 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
01:25Antianginal 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...
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
01:16Antianginal 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....
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