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

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

Antihypertensive Drugs: Angiotensin II Receptor Blockers

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...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

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,...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...

You might also read

Related Articles

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

Sort by
Same author

Long-term eculizumab treatment failure in C3 glomerulonephritis: two case reports.

Clinical kidney journal·2026
Same author

Limitations of Serum Bicarbonate as a Criterion for Metabolic Acidosis in CKD: Implications for Clinical Trials.

Journal of the American Society of Nephrology : JASN·2026
Same author

Baseline and follow-up association between adiposity and renal function: data from the ILERVAS cohort.

Obesity facts·2026
Same author

Severe Acute Hypertension Causes Hemolysis With Release of PEP and ACE Inhibitor.

Hypertension (Dallas, Tex. : 1979)·2026
Same author

A nephrology perspective on the clinical impact and management of delayed high-dose methotrexate elimination.

Expert review of anticancer therapy·2026
Same author

Short-Term Dietary Potassium Deprivation Induces Intense Kidney Sodium Retention.

Circulation research·2026

Related Experiment Video

Updated: Jul 2, 2026

Targeted Knockdown of Genes in the Choroid Plexus
04:43

Targeted Knockdown of Genes in the Choroid Plexus

Published on: June 16, 2023

Pharmacologic modulation of ACE2 expression.

María José Soler1, Clara Barrios, Raymond Oliva

  • 1Division of Nephrology and Hypertension, Department of Medicine, Feinberg School of Medicine, Northwestern University, 320 East Superior, Chicago, IL 60611, USA.

Current Hypertension Reports
|September 9, 2008
PubMed
Summary
This summary is machine-generated.

Angiotensin-converting enzyme 2 (ACE2) plays a role in kidney health. Modulating ACE2 expression through pharmacologic interventions may offer new treatments for kidney disease and hypertension.

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

Related Experiment Videos

Last Updated: Jul 2, 2026

Targeted Knockdown of Genes in the Choroid Plexus
04:43

Targeted Knockdown of Genes in the Choroid Plexus

Published on: June 16, 2023

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

Area of Science:

  • Biochemistry
  • Nephrology
  • Pharmacology

Background:

  • Angiotensin-converting enzyme 2 (ACE2) is a homologue of angiotensin-converting enzyme.
  • ACE2 degrades angiotensin I, angiotensin II, and other peptides.
  • Pathologic conditions can alter ACE2 expression in the kidney.

Purpose of the Study:

  • To review pharmacologic interventions that modulate ACE2 expression.
  • To explore the therapeutic potential of ACE2 in kidney disease and hypertension.

Main Methods:

  • Literature review of recent studies.
  • Focus on pharmacologic interventions targeting ACE2.

Main Results:

  • ACE2 expression is altered in the kidney under pathologic conditions.
  • Pharmacologic modulation of ACE2 is being investigated.

Conclusions:

  • ACE2 amplification shows potential as a therapeutic strategy for kidney disease.
  • ACE2 modulation may be beneficial for hypertension treatment.