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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

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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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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.
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Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
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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...

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Related Experiment Video

Updated: Jul 5, 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

Update on tissue renin-angiotensin systems.

Michael Bader1, Detlev Ganten

  • 1Max-Delbrück-Centrum for Molecular Medicine (MDC), Berlin, Germany. mbader@mdc-berlin.de

Journal of Molecular Medicine (Berlin, Germany)
|April 17, 2008
PubMed
Summary

Local tissue renin-angiotensin systems (RAS) amplify circulating Angiotensin II (Ang II) actions in organs like the heart and kidney. Transgenic models reveal tissue RAS importance in cardiovascular health and disease.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Biology
  • Endocrinology

Background:

  • Angiotensin II (Ang II) is produced both in circulation and locally within organs.
  • Mast cells also contribute to local Ang II production.
  • Local Ang II production is referred to as "tissue" renin-angiotensin system (RAS).

Purpose of the Study:

  • To review recent findings on the functional importance of tissue RAS.
  • To highlight the role of tissue RAS in cardiovascular organs.
  • To discuss implications for cardiovascular physiology and pathophysiology.

Main Methods:

  • Utilized transgenic rodent models with tissue-specific overexpression or deficiency of RAS components.
  • Analyzed findings from pharmacological experiments (though limited for tissue targeting).

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Related Experiment Videos

Last Updated: Jul 5, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
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A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

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  • Synthesized data from various studies on local RAS functions.

    • Main Results:

    • Local RAS amplify the effects of circulating Ang II in most tissues.
    • Tissue RAS play a significant role in cardiovascular physiology.
    • Dysregulation of tissue RAS is implicated in cardiovascular diseases.

    Conclusions:

    • Tissue RAS are crucial for local Ang II actions, impacting cardiovascular health.
    • Transgenic models are vital for understanding tissue-specific RAS functions.
    • Further research into tissue RAS is essential for understanding and treating cardiovascular diseases.