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

1.9K
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...
1.9K
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

1.6K
Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
1.6K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

1.9K
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...
1.9K
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

2.7K
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,...
2.7K
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

4.8K
Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
4.8K
Aortic Regurgitation III: Medical Management01:25

Aortic Regurgitation III: Medical Management

598
Aortic regurgitation (AR) is when the aortic valve does not close or seal properly, leading to backward blood circulation from the aorta into the left ventricle during diastole. Common causes of AR include rheumatic heart disease, congenital valve defects, and aortic root dilation. Managing AR requires a multifaceted approach to alleviate symptoms, preserve left ventricular function, and address the underlying cause of the regurgitation. Patients with symptomatic AR or significant left...
598

You might also read

Related Articles

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

Sort by
Same author

Ultrastructural changes in cryopreserved tracheal grafts of sprague-dawley rats.

ASAIO journal (American Society for Artificial Internal Organs : 1992)·2009
Same author

Facile synthesis of size-tunable micro-octahedra via metal-organic coordination.

Chemical communications (Cambridge, England)·2009
Same author

N-acetyl cysteine and penicillamine induce apoptosis via the ER stress response-signaling pathway.

Molecular carcinogenesis·2009
Same author

Targeting glucosylceramide synthase downregulates expression of the multidrug resistance gene MDR1 and sensitizes breast carcinoma cells to anticancer drugs.

Breast cancer research and treatment·2009
Same author

N-glycosylation of ATF6beta is essential for its proteolytic cleavage and transcriptional repressor function to ATF6alpha.

Journal of cellular biochemistry·2009
Same author

A humanized anti-osteopontin antibody inhibits breast cancer growth and metastasis in vivo.

Cancer immunology, immunotherapy : CII·2009

Related Experiment Video

Updated: May 4, 2026

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
06:18

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause

Published on: August 13, 2019

11.7K

Role of estrogen in diastolic dysfunction.

Zhuo Zhao1, Hao Wang, Jewell A Jessup

  • 1Department of Cardiology, Jinan Central Hospital, Affiliated with Shandong University, Jinan, China;

American Journal of Physiology. Heart and Circulatory Physiology
|January 14, 2014
PubMed
Summary

Estrogen loss after menopause increases the risk of diastolic dysfunction and heart failure in women. Estrogen, acting via GPR30, may protect the heart by modulating the renin-angiotensin-aldosterone system and nitric oxide synthase pathways.

Keywords:
Doppler echocardiographyG protein-coupled receptor 30diastolic dysfunctionestrogenmRen2sex differences

More Related Videos

Quantification of Global Diastolic Function by Kinematic Modeling-based Analysis of Transmitral Flow via the Parametrized Diastolic Filling Formalism
11:04

Quantification of Global Diastolic Function by Kinematic Modeling-based Analysis of Transmitral Flow via the Parametrized Diastolic Filling Formalism

Published on: September 1, 2014

10.6K
Noninvasive Determination of Vortex Formation Time Using Transesophageal Echocardiography During Cardiac Surgery
04:48

Noninvasive Determination of Vortex Formation Time Using Transesophageal Echocardiography During Cardiac Surgery

Published on: November 28, 2018

7.0K

Related Experiment Videos

Last Updated: May 4, 2026

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
06:18

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause

Published on: August 13, 2019

11.7K
Quantification of Global Diastolic Function by Kinematic Modeling-based Analysis of Transmitral Flow via the Parametrized Diastolic Filling Formalism
11:04

Quantification of Global Diastolic Function by Kinematic Modeling-based Analysis of Transmitral Flow via the Parametrized Diastolic Filling Formalism

Published on: September 1, 2014

10.6K
Noninvasive Determination of Vortex Formation Time Using Transesophageal Echocardiography During Cardiac Surgery
04:48

Noninvasive Determination of Vortex Formation Time Using Transesophageal Echocardiography During Cardiac Surgery

Published on: November 28, 2018

7.0K

Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Reproductive Biology

Background:

  • Left ventricular diastolic dysfunction (LVDD) prevalence rises post-menopause, potentially leading to heart failure.
  • Estrogen's cardioprotective mechanisms against hypertension and ventricular remodeling, especially in LVDD, are not fully understood.
  • The role of estrogen in cardiovascular disease, particularly LVDD, remains debated, with implications for postmenopausal women.

Purpose of the Study:

  • To investigate the mechanisms by which estrogen influences the renin-angiotensin-aldosterone system (RAAS) and nitric oxide synthase (NOS) pathways in the context of LVDD.
  • To explore the role of G protein-coupled receptor 30 (GPR30) in mediating estrogen's effects on cardiac function and related signaling pathways.
  • To understand the relationship between estrogen, GPR30, RAAS, NOS, and LVDD for potential therapeutic target identification.

Main Methods:

  • Utilized rodent models, specifically ovariectomized congenic mRen2.Lewis female rats, to mimic postmenopausal estrogen deficiency.
  • Examined the modulation of tissue RAAS and NOS systems by estrogen and its interaction with intracellular signaling pathways, including via GPR30.
  • Briefly discussed echocardiographic correlates and limitations for assessing LVDD in preclinical rodent studies.

Main Results:

  • Estrogen influences tissue RAAS and NOS systems and related intracellular signaling pathways, partly through GPR30.
  • Rodent models lacking estrogen exhibit cardiac phenotypes relevant to postmenopausal women.
  • Evidence suggests estrogen modulates pathways implicated in female sex-specific hypertensive heart disease.

Conclusions:

  • Estrogen plays a significant role in modulating the RAAS and NOS systems, impacting cardiac function.
  • GPR30 is a key mediator of estrogen's cardiovascular effects, offering a potential therapeutic target.
  • Understanding these interactions is crucial for developing treatments for diastolic heart failure that replicate estrogen's benefits without its risks.