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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...
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...
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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Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
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Related Experiment Video

Updated: Jun 7, 2026

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

Endothelin-1 expression in scleroderma renal crisis.

Luc Mouthon1, Marion Mehrenberger, Luis Teixeira

  • 1Université Paris Descartes, faculté de Médecine Paris Descartes, pôle de Médecine Interne, hôpital Cochin, Centre de référence pour les vascularites nécrosantes et la sclérodermie systémique, Assistance Publique-Hôpitaux de Paris (AP-HP), 75014 Paris, France. luc.mouthon@cch.aphp.fr

Human Pathology
|October 26, 2010
PubMed
Summary

Endothelin-1 is overexpressed in the kidneys of patients with scleroderma renal crisis, indicating its potential as a therapeutic target. This finding highlights the role of endothelin-1 in systemic sclerosis pathogenesis.

Related Experiment Videos

Last Updated: Jun 7, 2026

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

Area of Science:

  • Nephrology
  • Pathology
  • Immunohistochemistry

Background:

  • Systemic sclerosis is an autoimmune disease characterized by fibrosis and vascular abnormalities.
  • Scleroderma renal crisis (SRC) is a severe complication of systemic sclerosis, leading to acute kidney injury.
  • The specific pathogenic mechanisms underlying SRC require further elucidation.

Purpose of the Study:

  • To investigate the role of endothelin-1 (ET-1) in the pathogenesis of scleroderma renal crisis.
  • To compare ET-1 expression in kidney biopsies from SRC patients with various kidney diseases.

Main Methods:

  • Immunohistochemical analysis using anti-endothelin-1 and anti-von Willebrand factor antibodies.
  • Comparison of kidney biopsies from patients with SRC, normal kidneys, and other kidney diseases (hemolytic uremic syndrome, antiphospholipid syndrome, diabetic nephropathy, cyclosporine toxicity, nephroangiosclerosis).

Main Results:

  • SRC kidney biopsies showed characteristic lesions including glomerular thickening, mesangiolysis, fibrin thrombi, arteriolar mucoid thickening, "onion-skin" lesions, and fibrinoid necrosis.
  • Endothelin-1 staining pattern in glomeruli and arterioles was specific for scleroderma renal crisis.
  • Distinct ET-1 staining patterns were observed in other kidney diseases, differentiating them from SRC.

Conclusions:

  • Endothelin-1 is significantly overexpressed in the glomeruli and arterioles of patients with scleroderma renal crisis.
  • These findings suggest that endothelin-1 plays a crucial role in the pathogenesis of SRC.
  • Endothelin-1 represents a potential therapeutic target for managing scleroderma renal crisis.