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Related Concept Videos

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

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 (ECE). Of...
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...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
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...
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: 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,...

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Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader
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Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

Endothelin receptor antagonists.

Martine Clozel1, Alessandro Maresta, Marc Humbert

  • 1Actelion Pharmaceuticals Ltd, Gewerbestrasse 16, 4123, Allschwil, Switzerland, martine.clozel@actelion.com.

Handbook of Experimental Pharmacology
|October 5, 2013
PubMed
Summary
This summary is machine-generated.

Pulmonary arterial hypertension (PAH) involves endothelin (ET), nitric oxide (NO), and prostacyclin pathways. Endothelin receptor antagonists (ERAs) are crucial for PAH treatment, with ongoing research into novel therapies.

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Published on: December 23, 2014

Area of Science:

  • Cardiovascular Medicine
  • Pulmonary Medicine
  • Pharmacology

Background:

  • Pulmonary arterial hypertension (PAH) pathogenesis involves three key pathways: endothelin (ET), nitric oxide (NO), and prostacyclin.
  • These pathways are critical targets for current PAH therapies, advancing treatment and understanding.
  • The ET system, acting through ETA and ETB receptors, significantly contributes to PAH pathophysiology.

Purpose of the Study:

  • To elucidate the role of the endothelin system in PAH pathogenesis.
  • To review experimental data on ET's involvement in PAH.
  • To examine the clinical efficacy and status of endothelin receptor antagonists (ERAs) in PAH treatment.

Main Methods:

  • Review of experimental data concerning the endothelin system in PAH.
  • Analysis of the pathophysiology of PAH focusing on the ET pathway.
  • Examination of clinical trial data for approved and investigational ERAs.

Main Results:

  • The ET system plays a well-established, detrimental role in PAH.
  • Endothelin receptor antagonists (ERAs) are a key component of PAH therapy.
  • A novel ERA has recently undergone Phase III clinical investigation.

Conclusions:

  • The ET pathway is central to PAH pathogenesis and a validated therapeutic target.
  • ERAs represent an important class of drugs for managing PAH.
  • Continued research and development of ERAs offer promise for improved PAH treatment outcomes.