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Related Concept Videos

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,...
Hormonal Regulation01:33

Hormonal Regulation

The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
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...
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Introduction to Urinary System

The urinary system consists of two kidneys, two ureters, the urinary bladder, and the urethra.
The kidneys are bean-shaped organs located in the retroperitoneal space, on either side of the vertebral column, between the T12 and L3 vertebrae. They are partially protected by the rib cage and surrounded by perirenal fat, which provides cushioning. They are responsible for urine formation and play critical roles in regulating blood pressure, electrolyte levels, and hormone production. The ureters...

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Updated: Jul 7, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
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Published on: June 7, 2016

Can we live without a functional renin-angiotensin system?

Pierre Corvol1, Annie Michaud, Olivier Gribouval

  • 1INSERM, and Collège de France, Paris, France. pierre.corvol@college-de-france.fr

Clinical and Experimental Pharmacology & Physiology
|March 1, 2008
PubMed
Summary

Genetic defects in the renin-angiotensin system are compatible with survival in mice but cause severe renal tubular dysgenesis (RTD) in humans, leading to perinatal death. Differences in kidney development timing explain the varied severity of this condition.

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Last Updated: Jul 7, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
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Published on: June 7, 2016

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Published on: May 26, 2022

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08:21

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

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Area of Science:

  • Nephrology
  • Genetics
  • Developmental Biology

Background:

  • The renin-angiotensin system (RAS) is crucial for blood pressure regulation and fluid balance.
  • Inactivation of RAS components in mice does not prevent survival but increases salt sensitivity.
  • Renal tubular dysgenesis (RTD) is a severe human developmental disorder of the kidneys, resulting in anuria and perinatal mortality.

Purpose of the Study:

  • To investigate the role of the renin-angiotensin system in renal development and the pathogenesis of renal tubular dysgenesis.
  • To compare the effects of RAS inactivation in mice with human RTD.

Main Methods:

  • Analysis of gene inactivation models in mice for renin, angiotensin-converting enzyme, angiotensinogen, and AT1 receptor.
  • Clinical and genetic analysis of human patients with familial RTD.
  • Comparative analysis of renal development (nephrogenesis) in mice and humans.

Main Results:

  • Mice lacking functional RAS components survive but exhibit salt depletion sensitivity.
  • Familial RTD, an autosomal recessive disorder, results from genetic defects in the RAS.
  • Human RTD cases show absent proximal tubules, renal artery hyperplasia, neonatal anuria, and death, with intense renin gene expression stimulation.
  • Neonatal anuria and death occur in RTD with complete RAS gene inactivation.

Conclusions:

  • Complete inactivation of the renin-angiotensin system leads to severe renal malformations and perinatal death in humans, unlike in mice.
  • The critical window for human nephrogenesis before birth makes it more vulnerable to RAS defects compared to mice, where nephrogenesis continues postnatally.
  • Genetic defects in the renin-angiotensin system are a primary cause of renal tubular dysgenesis in humans.