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Related Concept Videos

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

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...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

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

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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

Antihypertensive Drugs: Angiotensin II Receptor Blockers

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

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

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...
Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

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. Administered...

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Related Experiment Video

Updated: May 27, 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

ACE inhibitor-induced angioedema.

Monali Vasekar1, Timothy J Craig

  • 1Department of Medicine, Penn State University, Hershey, PA 17033, USA. mvasekar@hmc.psu.edu

Current Allergy and Asthma Reports
|December 1, 2011
PubMed
Summary

Angiotensin-converting enzyme inhibitor-induced angioedema (ACEiIA) is more common than hereditary angioedema (HAE). This review explores ACEiIA management, including novel therapies investigated for HAE.

Area of Science:

  • Pharmacology
  • Immunology
  • Internal Medicine

Background:

  • Hereditary angioedema (HAE) has extensive literature, but angiotensin-converting enzyme inhibitor-induced angioedema (ACEiIA) is more prevalent.
  • Current HAE therapies are numerous, yet ACEiIA lacks a definitive treatment strategy.

Purpose of the Study:

  • To review the mechanism, prevalence, pathophysiology, and management of ACEiIA.
  • To evaluate the potential efficacy of novel HAE therapies for ACEiIA treatment.

Main Methods:

  • Literature review focusing on ACEiIA and HAE.
  • Analysis of recent therapeutic advancements in HAE.
  • Discussion of applying HAE treatments to ACEiIA.

Main Results:

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Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery
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Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery

Published on: December 23, 2014

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Last Updated: May 27, 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

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

  • ACEiIA affects a larger population than HAE.
  • No specific therapy currently exists for ACEiIA.
  • Newer HAE therapies show potential for ACEiIA management.

    • Conclusions:

    • There is a critical need for effective ACEiIA therapies.
    • Investigating HAE treatments offers a promising avenue for managing ACEiIA.
    • Further research is warranted to establish optimal treatment protocols for ACEiIA.