Related Experiment Video

Updated: Mar 9, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
12:03

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

18.5K

Angiotensin II-AT1-receptor signaling is necessary for cyclooxygenase-2-dependent postnatal nephron generation

Stefanie Frölich1, Patrick Slattery1, Dominique Thomas1

  • 1Institute of Clinical Pharmacology, Johann Wolfgang Goethe-University, Frankfurt, Germany.

Kidney International
|January 2, 2017
PubMed

Insights

Cyclooxygenase-2 (COX-2) is crucial for kidney development. Blocking the renin-angiotensin system impairs kidney maturation in mice, but activating angiotensin II-AT1 receptors can rescue function and reduce damage in COX-2 deficient kidneys.

Area of Science:

  • Nephrology
  • Developmental Biology
  • Pharmacology

Background:

  • Cyclooxygenase-2 (COX-2) plays a vital role in postnatal kidney development.
  • The renin-angiotensin system's involvement in COX-2-dependent nephrogenesis is not fully understood.

Purpose of the Study:

  • To investigate the contribution of the renin-angiotensin system to COX-2-dependent kidney development in mice.
  • To determine if impaired renal development and function in COX-2 deficient mice can be rescued.

Main Methods:

  • Administered angiotensin II receptor AT1 antagonist telmisartan, AT2 receptor antagonist PD123319, renin inhibitor aliskiren, and ACE inhibitor enalapril to mouse pups.
  • Administered AT1 receptor agonist L162313 to COX-2 deficient (COX-2-/-) mouse pups.
  • Assessed renal development, glomerular morphology, renal function (serum urea, creatinine), albumin excretion, and glomerulosclerosis.

Main Results:

  • Telmisartan treatment during critical postnatal periods mimicked the renal defects observed in COX-2-/- mice, including hypoplastic glomeruli and maturational arrest.
  • Inhibition of the renin-angiotensin system by aliskiren and enalapril also caused similar glomerular defects.
  • L162313 administration improved kidney growth, ameliorated renal defects, rescued impaired renal function, and reduced glomerulosclerosis in COX-2-/- mice, though it did not increase cortical mass.

Conclusions:

  • Angiotensin II-AT1 receptor signaling is essential for normal COX-2-dependent postnatal kidney development and maturation.
  • Targeting the renin-angiotensin system, specifically the AT1 receptor, holds potential for therapeutic intervention in conditions with impaired nephrogenesis.
Keywords:
cyclooxygenasenephrogenesisprostaglandinrenin angiotensin system

More Related Videos

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice07:21

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

39.6K
Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli12:19

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli

Published on: June 27, 2015

11.7K

Related Concept Videos

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...
2.9K
Endocrine Signaling01:45

Endocrine Signaling

Endocrine cells produce hormones to communicate with remote target cells found in other organs. The hormone reaches these distant areas using the circulatory system. This exposes the whole organism to the hormone but only those cells expressing hormone receptors or target cells are affected. Thus, endocrine signaling induces slow responses from its target cells but these effects also last longer.
68.7K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
3.8K
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...
2.7K
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.
36.6K
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,...
1.7K