Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

890
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,...
890
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

1.0K
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...
1.0K
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

1.1K
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...
1.1K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

558
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...
558
Hormonal Regulation01:33

Hormonal Regulation

34.0K
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.
34.0K
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

715
β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this,...
715

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Exaggerating the risks of vaccination is a dangerous health threat.

BioImpacts : BI·2026
Same author

Is Alzheimer's an Autoimmune Disease?

Molecular neurobiology·2026
Same author

Chronic Treatment of a Mouse Model of Cerebral Amyloid Angiopathy and Brain AT<sub>1</sub> Receptor Expression.

bioRxiv : the preprint server for biology·2025
Same author

Comparative evaluation of biased agonists Sarcosine<sup>1</sup> , d-Alanine<sup>8</sup> -Angiotensin (Ang) II (SD Ang II) and Sarcosine<sup>1</sup> , Isoleucine<sup>8</sup> -Ang II (SI Ang II) and their radioiodinated congeners binding to rat liver membrane AT<sub>1</sub> receptors.

Pharmacology research & perspectives·2023
Same author

CGP42112: the full AT2 receptor agonist and its role in the renin-angiotensin-aldosterone system: no longer misunderstood.

Clinical science (London, England : 1979)·2022
Same author

An opinion on the impacts of COVID-19 worldwide.

BioImpacts : BI·2022

Related Experiment Video

Updated: Oct 10, 2025

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

18.1K

Countering the classical renin-angiotensin system.

Natalia M Noto1, Yazmin M Restrepo1, Robert C Speth1

  • 1College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL 33328, U.S.A.

Clinical Science (London, England : 1979)
|December 8, 2021
PubMed
Summary

Angiotensin-(1-7) [Ang-(1-7)] peptide has therapeutic potential but is rapidly metabolized. A new transgenic rat model overexpressing an Ang-(1-7)-producing fusion protein offers a solution, though potential concerns warrant discussion.

Keywords:
Angiotensin-(1-7)Cardiovascular SystemRenin-Angiotensin SystemSympathetic Nervous SystemTransgenic RatVasopressin

More Related Videos

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

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

Published on: October 26, 2020

5.1K
Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

3.6K

Related Experiment Videos

Last Updated: Oct 10, 2025

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

18.1K
A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

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

Published on: October 26, 2020

5.1K
Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

3.6K

Area of Science:

  • Cardiovascular Physiology
  • Endocrinology
  • Pharmacology

Background:

  • Angiotensin-(1-7) [Ang-(1-7)] exhibits opposing effects to Angiotensin II (Ang II) in the periphery, while mimicking Ang II in the brain.
  • Ang-(1-7) interacts with various receptors, influencing vasopressin release and cardiovascular function.
  • The rapid metabolic breakdown of Ang-(1-7) limits its therapeutic applications.

Purpose of the Study:

  • To introduce and discuss a novel transgenic rat model designed to overcome the metabolic instability of Ang-(1-7).
  • To evaluate the potential benefits and challenges associated with this new model for Ang-(1-7) research and therapy.

Main Methods:

  • Development of a transgenic rat model overexpressing a fusion protein that produces Ang-(1-7).
  • Commentary and analysis of the implications of this model in the context of existing knowledge on the renin-angiotensin system.

Main Results:

  • The study presents a technical advancement in creating a model for sustained Ang-(1-7) production.
  • This model circumvents the rapid inactivation issue, potentially enabling new therapeutic strategies.

Conclusions:

  • The developed transgenic rat model represents a significant step forward for studying Ang-(1-7) in vivo.
  • Further discussion and investigation are needed to address potential concerns and fully leverage the advances offered by this model.