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

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,...
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...
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-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: Action of Diuretics01:16

Antihypertensive Drugs: Action of Diuretics

Diuretics are antihypertensive drugs used to treat hypertension resulting from sodium and water retention. Sodium, vital for fluid balance and nerve or muscle function, is regulated by the kidneys through millions of nephrons. Blood enters nephrons via afferent arterioles, which branch into capillaries called glomeruli. These filter blood plasma, allowing water and solutes, like sodium ions, to pass through capillary walls into Bowman's capsule. The filtrate then flows through various tubules...
Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...

You might also read

Related Articles

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

Sort by
Same author

Chemerin knockout reveals sex difference in the role of chemerin in blood pressure and vascular remodeling.

American journal of physiology. Heart and circulatory physiology·2026
Same author

Editorial: Unraveling the influence of perivascular adipose tissue on vascular health.

Frontiers in physiology·2026
Same author

Presence and Variability of the Microbiome in Perivascular Adipose Tissue: A Whole-Genome Sequencing Study in Dahl SS Rats.

Life (Basel, Switzerland)·2026
Same author

Nuclei isolation from rat and cow white adipose tissues for single-nucleus RNA sequencing; rat WAT remains a challenge.

Frontiers in physiology·2026
Same author

Surgical Induction of Mid-Thoracic Aortic Coarctation in Mice: A Reproducible Preclinical Model of Pressure-Induced Vascular Remodeling.

Current protocols·2026
Same author

Biomechanical adaptation of the thoracic aorta and its perivascular adipose tissue precedes hypertension development in Dahl Salt-Sensitive rats on high-fat diet.

Acta biomaterialia·2026

Related Experiment Video

Updated: Jun 8, 2026

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

Allopurinol does not decrease blood pressure or prevent the development of hypertension in the deoxycorticosterone

Theodora Szasz1, A Elizabeth Linder, Robert P Davis

  • 1Pharmacology and Toxicology Department, Michigan State University, East Lansing, MI 48824-1317, USA. szasziri@msu.edu

Journal of Cardiovascular Pharmacology
|October 1, 2010
PubMed
Summary

Xanthine oxidase (XO) inhibition using allopurinol did not affect blood pressure in a rat model of deoxycorticosterone acetate-salt hypertension. This suggests XO does not play a significant role in this hypertension model.

Related Experiment Videos

Last Updated: Jun 8, 2026

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:

  • Cardiovascular Research
  • Renal Physiology
  • Oxidative Stress Biology

Background:

  • Hypertension is linked to increased reactive oxygen species (ROS) and oxidative stress.
  • Xanthine oxidase (XO) is a key enzyme producing ROS, with potential implications in hypertension.
  • Previous studies on XO inhibition's effect on blood pressure show conflicting results.

Purpose of the Study:

  • To investigate if XO inhibition decreases blood pressure or prevents deoxycorticosterone acetate (DOCA)-salt hypertension development.
  • To evaluate the role of XO in established and developing DOCA-salt hypertension in rats.

Main Methods:

  • Administration of allopurinol (XO inhibitor) or vehicle to rats during DOCA-salt hypertension.
  • Validation of XO inhibition via HPLC analysis of urinary and serum metabolites.
  • Continuous blood pressure monitoring using radiotelemetry and organ evaluation.

Main Results:

  • Allopurinol treatment did not alter the progression of DOCA-salt hypertension.
  • No significant positive differences were observed between allopurinol and vehicle groups, except for a decrease in pulse pressure.
  • XO inhibition did not impact target organs of hypertension.

Conclusions:

  • Xanthine oxidase does not appear to play a critical role in the development or maintenance of DOCA-salt hypertension in this rat model.
  • Further research may be needed to clarify the specific role of XO in different forms of hypertension.