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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,...
Glomerular Filtration Rate and its Regulation01:28

Glomerular Filtration Rate and its Regulation

The Glomerular Filtration Rate (GFR) is a measure of kidney function, reflecting the volume of filtrate formed per minute in the kidneys. On average, GFR is approximately 125 mL/min in males and 105 mL/min in females. Maintaining a relatively constant GFR is essential for the kidneys to effectively regulate body fluid homeostasis and maintain extracellular stability.
GFR regulation involves two primary intrinsic controls: the myogenic and tubuloglomerular feedback mechanisms.
The myogenic...
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...
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.
Renal Regulation of Acid-Base Balance01:29

Renal Regulation of Acid-Base Balance

Metabolic reactions in the body produce nonvolatile acids, such as sulfuric acid, which generate an acid load of approximately 1 mEq of H+ per kilogram of body weight daily. Excreting H+ in the urine is essential to balance this acid load.
In the kidneys, cells within the proximal convoluted tubules (PCT) and the collecting ducts secrete hydrogen ions (H+) into the tubular fluid. Specifically, in the PCT, Na+/H+ antiporters secrete H+ while reabsorbing Na+.
However, the intercalated cells in...

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Related Experiment Video

Updated: Jun 23, 2026

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
10:15

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection

Published on: November 10, 2021

Relaxin: an endogenous renoprotective factor?

Tim D Hewitson1, Chrishan S Samuel

  • 1Department of Nephrology, The Royal Melbourne Hospital, Melbourne, Australia. Tim.Hewitson@mh.org.au

Annals of the New York Academy of Sciences
|May 7, 2009
PubMed
Summary

Relaxin, an antifibrotic factor, protects kidneys by counteracting scarring signals. Its absence accelerates kidney fibrosis, but treatment with H2 relaxin reverses this damage.

Area of Science:

  • Nephrology and cellular biology
  • Pathology of organ scarring

Background:

  • Fibrosis, or scarring, is a major cause of organ dysfunction and pathology.
  • Renal fibrosis involves excessive extracellular matrix accumulation, leading to kidney failure.
  • Fibroblasts are key cells in renal fibrosis, regulated by profibrotic factors like TGF-β.

Purpose of the Study:

  • To review the cellular and molecular mechanisms of fibrosis.
  • To highlight the role of endogenous antifibrotic factors, specifically relaxin.
  • To discuss how relaxin influences fibrotic processes in the kidney.

Main Methods:

  • Review of recent scientific literature on renal fibrosis and relaxin.
  • Analysis of cellular and molecular mechanisms underlying fibrotic disease.

Related Experiment Videos

Last Updated: Jun 23, 2026

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
10:15

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection

Published on: November 10, 2021

  • Examination of the effects of relaxin deficiency and supplementation.

    • Main Results:

    • Absence of endogenous relaxin leads to spontaneous age-related fibrosis and accelerated injury-induced fibrosis.
    • Recombinant H2 relaxin administration reverses these fibrotic effects.
    • Relaxin acts as a renoprotective factor by counteracting profibrotic signals.

    Conclusions:

    • Relaxin is a critical endogenous antifibrotic factor with therapeutic potential for kidney disease.
    • Understanding relaxin's mechanisms can lead to new strategies for preventing and treating renal fibrosis.
    • Targeting relaxin pathways may offer a novel approach to managing progressive kidney damage.