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

Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

1.2K
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,...
1.2K
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

2.9K
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...
2.9K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

2.7K
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...
2.7K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

1.3K
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...
1.3K
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

2.4K
Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
2.4K
Hypertension and Regulation of Blood Pressure01:18

Hypertension and Regulation of Blood Pressure

4.6K
Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
4.6K

You might also read

Related Articles

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

Sort by
Same author

Mitoquinone Prevents Cardiac Dysfunction by Normalizing Mitochondrial ROS and Calcium Handling in Acute Myocardial Infarction.

Acta physiologica (Oxford, England)·2026
Same author

Bariatric surgery reverses blunted blood pressure reactivity to cold-induced stress in patients with severe obesity.

Obesity research & clinical practice·2026
Same author

Red quinoa hydrolysate as a plant-based therapeutic alternative for damage induced by high cadmium concentrations to the vascular system in rats.

Food & function·2026
Same author

Intraorbital optic nerve coloboma: Neurosurgical considerations from two rare cases.

Surgical neurology international·2025
Same author

A Refined Carbohydrate-Rich Diet Reduces Vascular Reactivity Through Endothelial Oxidative Stress and Increased Nitric Oxide: The Involvement of Inducible Nitric Oxide Synthase.

Nutrients·2025
Same author

Chronic Mercury Exposure Triggers Vascular Remodeling and Impaired Vasoconstriction in Small Intrapulmonary Arteries.

Cardiovascular toxicology·2025

Related Experiment Video

Updated: Mar 3, 2026

Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
10:18

Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model

Published on: June 29, 2014

17.6K

A Single Resistance Exercise Session Improves Aortic Endothelial Function in Hypertensive Rats.

Thaís de Oliveira Faria1, Jhuli Keli Angeli1, Luiz Guilherme Marchesi Mello1

  • 1Universidade Federal do Espírito Santo, Vitória, ES, Brazil.

Arquivos Brasileiros De Cardiologia
|April 27, 2017
PubMed
Summary

A single session of dynamic resistance exercise enhanced endothelial function in hypertensive rats. This improvement is linked to increased nitric oxide production via endothelial nitric oxide synthase activation.

More Related Videos

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
07:31

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats

Published on: December 2, 2016

10.8K
A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats
07:41

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats

Published on: March 1, 2022

3.5K

Related Experiment Videos

Last Updated: Mar 3, 2026

Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
10:18

Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model

Published on: June 29, 2014

17.6K
A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
07:31

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats

Published on: December 2, 2016

10.8K
A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats
07:41

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats

Published on: March 1, 2022

3.5K

Area of Science:

  • Physiology
  • Cardiovascular Research
  • Exercise Science

Background:

  • Physical exercise is recognized for its positive impact on endothelial function.
  • Endothelial dysfunction is a hallmark of hypertension.
  • Spontaneously hypertensive rats (SHR) serve as a model for studying hypertension-related cardiovascular changes.

Purpose of the Study:

  • To investigate the acute effects of dynamic resistance exercise on endothelial function in spontaneously hypertensive rats.
  • To examine the molecular mechanisms underlying exercise-induced changes in endothelial function.

Main Methods:

  • Aortic rings from exercised and control spontaneously hypertensive rats were analyzed.
  • Expression levels of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS1177), and inducible nitric oxide synthase (iNOS) were assessed.
  • Vascular reactivity to acetylcholine (vasodilator) and phenylephrine (vasoconstrictor) was evaluated.

Main Results:

  • Acute resistance exercise significantly improved acetylcholine-induced vasodilation in aortic rings.
  • Exercise reduced the maximal response to phenylephrine, indicating altered vascular tone regulation.
  • Increased phosphorylation of eNOS (p-eNOS1177) was observed post-exercise, suggesting enhanced nitric oxide signaling.

Conclusions:

  • A single bout of dynamic resistance exercise can acutely improve endothelial function in hypertensive rats.
  • The beneficial effects appear to be mediated by enhanced nitric oxide production through eNOS activation.
  • These findings highlight the potential of acute exercise as an intervention for managing hypertension-related endothelial dysfunction.