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Related Concept Videos

Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
Regulation of Metabolism01:19

Regulation of Metabolism

Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...
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...
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.

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Related Experiment Video

Updated: Jun 5, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Reprogrammed Propionate Metabolism Alters Redox-Dependent Aldosterone Production.

Min Sun1, Maoting Gao1, Yuqing Liu1

  • 1Department of Endocrinology (M.S., M.G., Y.L., Z.X., M.Z., C.W., T.Y., Y.Y.), The First Affiliated Hospital With Nanjing Medical University, China.

Hypertension (Dallas, Tex. : 1979)
|June 4, 2026
PubMed
Summary
This summary is machine-generated.

Metabolic reprogramming in aldosterone-producing adenomas involves propionate metabolism, leading to excess aldosterone. This pathway highlights methylmalonic acid, oxidative stress, and calcium channel modification as key drivers.

Keywords:
adrenal glandcalciumcalmodulinmethylmalonic acidoxidative stress

Related Experiment Videos

Last Updated: Jun 5, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Area of Science:

  • Endocrinology
  • Metabolic Biology
  • Oncology

Background:

  • Metabolic reprogramming is a key factor in endocrine tumors.
  • The specific metabolic alterations driving aldosterone excess in aldosterone-producing adenomas are not well understood.

Purpose of the Study:

  • To investigate metabolic reprogramming in aldosterone-producing adenomas.
  • To elucidate the mechanisms linking metabolic dysregulation to aldosterone overproduction.

Main Methods:

  • Multiomics profiling of human adrenal and blood samples.
  • Validation of metabolic intermediates in adenomas.
  • Functional studies in adrenocortical cells and mice.
  • Transcriptomics, mass spectrometry, and functional assays.

Main Results:

  • Aldosterone-producing adenomas show altered propionate metabolism with methylmalonic acid accumulation, linked to PCCA upregulation.
  • PCCA overexpression and methylmalonic acid increase aldosterone synthase (CYP11B2) expression and aldosterone production.
  • Methylmalonic acid induces oxidative stress, leading to Cav1.2 channel S-glutathionylation, enhancing its activity and driving aldosterone production.

Conclusions:

  • A novel methylmalonic acid-oxidative stress-Cav1.2 S-glutathionylation axis connects metabolic changes to aldosterone production.
  • This pathway offers potential therapeutic targets for primary aldosteronism by modulating redox-dependent metabolic signaling.