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: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

617
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...
617
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

711
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...
711
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

427
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,...
427
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

421
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...
421
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

585
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,...
585
Hormonal Regulation01:33

Hormonal Regulation

33.1K
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.
33.1K

You might also read

Related Articles

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

Sort by
Same author

Vascular Endothelial Growth Factor Receptors 1 and 3 Mediate Placental Trophoblast Leptin Production in Preeclampsia, Inducing Vascular Dysfunction.

Arteriosclerosis, thrombosis, and vascular biology·2026
Same author

Ex situ heart perfusion: a novel model for drug validation and translation.

Frontiers in cardiovascular medicine·2026
Same author

Psychological and Physical Readiness Profiles for Return to Sport in Patients After Anterior Cruciate Ligament Reconstruction: An Analysis of 822 Patients.

Orthopaedic journal of sports medicine·2026
Same author

Predictors of survival after penetrating cardiac trauma: injury patterns and presentation factors.

Trauma surgery & acute care open·2026
Same author

Integrative Molecular Analyses of Inflammatory and Autoimmune Signals in Cardiac Sarcoidosis.

Circulation·2026
Same author

Supervised machine learning identifies impaired mitochondrial quality control in β-cells with development of type 2 diabetes.

NPJ systems biology and applications·2026

Related Experiment Video

Updated: Jun 24, 2025

Assessing Murine Resistance Artery Function Using Pressure Myography
07:25

Assessing Murine Resistance Artery Function Using Pressure Myography

Published on: June 7, 2013

22.1K

UBR1 Promotes Sex-Dependent ACE2 Ubiquitination in Hypertension.

Mona Elgazzaz, Navya Lakkappa, Clara Berdasco

    Medrxiv : the Preprint Server for Health Sciences
    |June 3, 2024
    PubMed
    Summary

    Researchers identified UBR1 as a novel E3 ligase that targets the antihypertensive enzyme ACE2 for degradation in hypertension. Targeting UBR1 and Nedd4-2 may restore ACE2 activity in hypertensive individuals.

    More Related Videos

    Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
    07:21

    Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

    Published on: September 28, 2015

    37.4K
    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

    4.7K

    Related Experiment Videos

    Last Updated: Jun 24, 2025

    Assessing Murine Resistance Artery Function Using Pressure Myography
    07:25

    Assessing Murine Resistance Artery Function Using Pressure Myography

    Published on: June 7, 2013

    22.1K
    Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
    07:21

    Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

    Published on: September 28, 2015

    37.4K
    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

    4.7K

    Area of Science:

    • Cardiovascular Biology
    • Molecular Endocrinology
    • Hypertension Research

    Background:

    • Angiotensin II (Ang-II) impairs antihypertensive enzyme ACE2 function, contributing to hypertension.
    • ACE2 ubiquitination and degradation are key mechanisms, but partners remain largely unknown.

    Approach:

    • Proteomics and bioinformatics identified ACE2 ubiquitination partners in Ang-II infused mice.
    • UBR1 interaction with ACE2 was validated in cells.
    • UBR1 knockdown was performed centrally and peripherally in male mice.

    Key Points:

    • Proteomics identified UBR1 as an E3 ligase promoting ACE2 ubiquitination in the hypothalamus.
    • UBR1 expression correlated with ACE2 reduction in hypertensive mice and humans.
    • Testosterone, not estradiol, mediated sex-specific UBR1 regulation.
    • UBR1 knockdown restored ACE2 levels and transiently reduced blood pressure in hypertensive males.
    • UBR1 knockdown affected Nedd4-2 and SGK1 pathways.

    Conclusions:

    • UBR1 is a novel ubiquitin ligase targeting ACE2 in hypertension.
    • UBR1 and Nedd4-2 may synergistically ubiquitinate ACE2.
    • Targeting these E3 ligases could restore ACE2 activity in hypertension.