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Related Concept Videos

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...
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...
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.
Introduction to Urinary System01:13

Introduction to Urinary System

The urinary system consists of two kidneys, two ureters, the urinary bladder, and the urethra.
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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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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...

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Related Experiment Video

Updated: May 29, 2026

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli
12:19

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

Published on: June 27, 2015

Endothelins and kidney acidification.

Donald E Wesson1

  • 1Texas A&amp;M Health Sciences Center College of Medicine, Scott and White Healthcare, Temple, Tex., USA.

Contributions to Nephrology
|September 7, 2011
PubMed
Summary

Endothelins (ETs) enhance kidney acidification and tubule function, particularly during acid challenges or reduced glomerular filtration rate (GFR). Increased kidney ET activity may also worsen chronic kidney disease progression.

Area of Science:

  • Nephrology
  • Physiology
  • Endocrinology

Background:

  • Endothelins (ETs) are known for vasoactivity but also impact kidney tubule transport.
  • ETs play a role in regulating kidney acidification.
  • Their role in chronic kidney disease (CKD) and metabolic alkalosis is increasingly recognized.

Purpose of the Study:

  • To investigate the physiological role of endothelins in kidney acidification.
  • To explore the pathophysiological consequences of increased kidney ET activity, especially in CKD.

Main Methods:

  • The study reviews existing literature on endothelins and kidney function.
  • Analysis of physiological and pathophysiological roles in various kidney conditions.

Main Results:

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Assessment of Vascular Function in Patients With Chronic Kidney Disease
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Assessment of Vascular Function in Patients With Chronic Kidney Disease

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Last Updated: May 29, 2026

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli
12:19

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

Published on: June 27, 2015

Two-photon Imaging of Intracellular Ca2+ Handling and Nitric Oxide Production in Endothelial and Smooth Muscle Cells of an Isolated Rat Aorta
08:08

Two-photon Imaging of Intracellular Ca2+ Handling and Nitric Oxide Production in Endothelial and Smooth Muscle Cells of an Isolated Rat Aorta

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Assessment of Vascular Function in Patients With Chronic Kidney Disease
08:50

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

  • ETs enhance kidney acidification in response to acid loads.
  • ETs promote tubule acidification in conditions of reduced glomerular filtration rate (GFR), such as in CKD.
  • Elevated kidney ET activity is implicated in the progression of certain nephropathies and in metabolic alkalosis.

Conclusions:

  • Endothelins are critical regulators of kidney acidification.
  • Increased kidney ET activity may contribute to CKD progression and other kidney diseases.
  • Further research is needed to fully elucidate the physiological and pathophysiological roles of ETs in kidney health and disease.