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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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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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Endocrinal or hormonal intervention in the cardiovascular system is predominantly exerted by the catecholamines - epinephrine and norepinephrine, as well as a slew of hormones that interact with renal function to modulate blood volume.
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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...
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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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Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
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Updated: May 24, 2025

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
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Renin-Angiotensin-Aldosterone System Profiling in Horses Before and After Exercise.

Todd Holbrook1, Jorge Hernandez1, Taralyn McCarrel1

  • 1College of Veterinary Medicine, University of Florida, Gainesville, Florida, USA.

Journal of Veterinary Internal Medicine
|March 6, 2025
PubMed
Summary

Exercise activates both the classical and alternative renin-angiotensin-aldosterone system (RAAS) pathways in horses. Both pathways showed increased metabolites and enzyme activity following physical exertion.

Keywords:
RAASenduranceexercisehorse

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Area of Science:

  • Equine physiology
  • Cardiovascular research
  • Endocrinology

Background:

  • The effects of exercise on the renin-angiotensin-aldosterone system (RAAS) in horses remain largely uninvestigated.
  • Understanding RAAS pathway responses to exercise is crucial for equine health and performance.

Purpose of the Study:

  • To determine if exercise activates classical and alternative RAAS pathways in horses.
  • To compare the activation of the classical RAAS pathway between endurance and high-intensity exercise.

Main Methods:

  • Blood samples were collected from 25 horses before and after four different exercise protocols.
  • Serum metabolites and enzyme activities of the RAAS pathways were measured using equilibrium analysis.
  • Comparisons were made between pre- and post-exercise values and among different exercise groups.

Main Results:

  • Exercise significantly increased classical RAAS metabolites (angiotensin I, angiotensin II, aldosterone) and alternative RAAS metabolites (angiotensin 1-7, angiotensin 1-5) in all horses.
  • Angiotensin-converting enzyme-2 activity also significantly increased post-exercise.
  • The angiotensin 1-7 ratio was notably higher in horses undergoing short-duration, high-intensity racing (TB-R) compared to endurance (A-E) and treadmill exercise (TB-TM).

Conclusions:

  • Both classical and alternative RAAS pathways are activated by exercise in horses.
  • Exercise significantly impacts RAAS metabolite levels and enzyme activity.
  • Different exercise types may elicit varying responses within the RAAS, particularly concerning the alternative pathway.