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 II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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...
Hormonal Regulation of Blood Pressure01:17

Hormonal Regulation of Blood Pressure

Endocrinal or hormonal intervention in the cardiovascular system is predominantly exerted by the catecholamines - epinephrine and norepinephrine, as well as a slew of hormones that interact with renal function to modulate blood volume.
Epinephrine and Norepinephrine
The adrenal medulla releases epinephrine and norepinephrine, catecholamines that enhance and extend the sympathetic or "fight or flight" physiological response. These hormones escalate heart rate and the force of contraction while...
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

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, β1-blockers...
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

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,...
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...

You might also read

Related Articles

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

Sort by
Same author

Evaluation of a novel phrase-based speech-recognition test using synthetic speech.

International journal of audiology·2026
Same author

The Relation Between Sustained Listening Under Difficult Conditions and Behavioral, Subjective, and Physiological Indicators of Fatigue.

Trends in hearing·2026
Same author

A revision of <i>Peronospora</i> species on <i>Veronica</i> unravels a species-rich group of downy mildew pathogens with host shifts to economically important ornamental plants.

IMA fungus·2026
Same author

Analysis of Spatial, Binaural, and Better-Ear Benefits for Different Degrees of Hearing Loss Using a Binaural Speech Intelligibility Model.

Trends in hearing·2026
Same author

Hold to continue - safety aspects of cooperative human machine systems in urban traffic.

Applied ergonomics·2025
Same author

Modelling context processing during sentence recognition in noise and reverberation for listeners with and without hearing loss.

The Journal of the Acoustical Society of America·2025

Related Experiment Video

Updated: Jun 21, 2026

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

ANP expression in the hypertensive heart.

Gania Kessler-Icekson1, Yael Barhum, Jutta Schaper

  • 1Basil and Gerald Felsenstein Medical Research Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel;

Experimental and Clinical Cardiology
|August 4, 2009
PubMed
Summary

Atrial natriuretic peptide (ANP) expression in hypertensive hearts is primarily controlled by hemodynamic state, not just hypertrophy. Myocyte cell size and ANP production appear to be independent features in hypertension.

Keywords:
Atrial natriuretic peptideGATA-4HypertensionHypertrophySpontaneously hypertensive rat

More Related Videos

Isolation of Atrial Myocytes from Adult Mice
08:34

Isolation of Atrial Myocytes from Adult Mice

Published on: July 25, 2019

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

Related Experiment Videos

Last Updated: Jun 21, 2026

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

Isolation of Atrial Myocytes from Adult Mice
08:34

Isolation of Atrial Myocytes from Adult Mice

Published on: July 25, 2019

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

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology

Background:

  • Atrial natriuretic peptide (ANP) is mainly produced in the atria but also in fetal ventricles.
  • Increased ANP expression in adult ventricles correlates with pressure-induced hypertrophy and fetal gene program activation.
  • ANP is a recognized marker for myocardial hypertrophy in conditions like chronic hypertension.

Purpose of the Study:

  • To investigate the relationship between hemodynamic state, cardiac hypertrophy, and ANP expression in hypertensive rat hearts.
  • To determine the role of the transcription factor GATA-4 in regulating ANP expression and hypertrophy under hypertension.
  • To explore the potential independence of myocyte cell size and ANP production in the hypertensive heart.

Main Methods:

  • Analysis of ANP expression and cardiac hypertrophy in hypertensive rat models.
  • Assessment of GATA-4 activity in relation to ANP levels and hypertrophy.
  • Correlation of hemodynamic parameters with ANP expression and myocyte characteristics.

Main Results:

  • A decrease in hypertension and ANP expression occurred while hypertrophy persisted, indicating hemodynamic state overrides hypertrophy in controlling ANP.
  • Reduced GATA-4 activity correlated with ANP downregulation but not with persistent hypertrophy.
  • These findings suggest that factors beyond GATA-4 activity contribute to maintaining cardiac hypertrophy.

Conclusions:

  • Hemodynamic state is a primary regulator of ANP expression in hypertensive hearts, more so than hypertrophy itself.
  • Cardiac hypertrophy maintenance in hypertension may involve additional factors beyond GATA-4.
  • Myocyte cell size and ANP production may be autonomous and independently regulated features in the hypertensive heart.