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

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: 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
Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

2.5K
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...
2.5K
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: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

1.7K
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,...
1.7K
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

1.0K
β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
1.0K

You might also read

Related Articles

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

Sort by
Same author

Inspiratory muscle training improves exercise performance and breathing pattern during 6-min walking test in systemic sclerosis-associated interstitial lung disease.

ERJ open research·2026
Same author

Interplay of pulmonary circulation, cardiac filling pressures, and sympathovagal balance in exercise-induced hyperventilation among cardiopulmonary disorders.

American journal of physiology. Regulatory, integrative and comparative physiology·2026
Same author

Effects of home-based inspiratory muscle training on sympatho-vagal balance, quality of life, and inflammatory profile in patients with systemic sclerosis-associated interstitial lung disease.

European journal of medical research·2026
Same author

Interactions between brown adipose tissue activity and exercise modality on metabolic kinetics: a crossover study in trained individuals.

Journal of thermal biology·2026
Same author

Combined nandrolone and resistance training induced cardiac remodelling and oxidative stress despite enhanced cardiomyocyte contractility.

PloS one·2026
Same author

Brazilian Guidelines of Hypertension - 2025.

Arquivos brasileiros de cardiologia·2025

Related Experiment Video

Updated: Mar 7, 2026

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

4.3K

Captopril does not Potentiate Post-Exercise Hypotension: A Randomized Crossover Study.

Andréia Cristiane Carrenho Queiroz1, Julio Cesar Silva Sousa1, Natan Daniel Silva1

  • 1School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil.

International Journal of Sports Medicine
|February 21, 2017
PubMed
Summary

Captopril did not enhance post-resistance exercise hypotension (PREH) in hypertensive men. This study found no significant differences in blood pressure reduction or underlying mechanisms between captopril and placebo treatments after exercise.

More Related Videos

Author Spotlight: Exploring Huotan Jiedu Tongluo Decoction as an Antihypertensive Drug
05:57

Author Spotlight: Exploring Huotan Jiedu Tongluo Decoction as an Antihypertensive Drug

Published on: May 17, 2024

1.3K
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

5.7K

Related Experiment Videos

Last Updated: Mar 7, 2026

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

4.3K
Author Spotlight: Exploring Huotan Jiedu Tongluo Decoction as an Antihypertensive Drug
05:57

Author Spotlight: Exploring Huotan Jiedu Tongluo Decoction as an Antihypertensive Drug

Published on: May 17, 2024

1.3K
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

5.7K

Area of Science:

  • Cardiovascular Physiology
  • Exercise Science
  • Pharmacology

Background:

  • Hypertension (HT) management often involves medication.
  • Post-resistance exercise hypotension (PREH) is a phenomenon where blood pressure decreases after resistance exercise.
  • The potential potentiation of PREH by antihypertensive medications requires investigation.

Purpose of the Study:

  • To determine if captopril potentiates post-resistance exercise hypotension (PREH) in hypertensive men.
  • To investigate the effects of captopril on the characteristics and mechanisms of PREH.
  • To compare PREH following resistance exercise with captopril versus placebo.

Main Methods:

  • A double-blinded, randomized-crossover study involving 12 hypertensive men.
  • Subjects received captopril (3x50 mg/day) and placebo for 4 weeks each.
  • Blood pressure and hemodynamic variables were measured during control and resistance exercise sessions, with 24-hour ambulatory monitoring.

Main Results:

  • Captopril did not alter the magnitude or duration of post-resistance exercise hypotension compared to placebo.
  • Systolic and diastolic blood pressure decreased similarly after resistance exercise in both treatment periods.
  • No significant differences were observed in the hemodynamic mechanisms underlying PREH between captopril and placebo conditions.

Conclusions:

  • Captopril does not potentiate post-resistance exercise hypotension in hypertensive men.
  • The antihypertensive medication captopril does not influence the mechanisms or extent of PREH.
  • Resistance exercise elicits hypotension independently of captopril treatment in this population.