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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...
Mitral Regurgitation I: Introduction01:20

Mitral Regurgitation I: Introduction

Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...
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...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

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...

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Related Experiment Video

Updated: Jun 21, 2026

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
07:13

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Published on: April 30, 2020

Left ventricular remodeling with exercise in hypertension.

Stephen C Kolwicz1, Scott M MacDonnell, Brian F Renna

  • 1Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|August 12, 2009
PubMed
Summary

Exercise training in hypertensive rats augmented cardiomyocyte size but reduced cell death and increased progenitor cells. This suggests exercise may promote a healthier heart in hypertension.

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Last Updated: Jun 21, 2026

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
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Published on: February 13, 2021

Area of Science:

  • Cardiovascular Physiology
  • Exercise Science
  • Hypertension Research

Background:

  • Chronic hypertension is associated with detrimental left ventricular remodeling.
  • Exercise training's impact on hypertensive cardiac remodeling, particularly cardiomyocyte changes, requires further elucidation.

Purpose of the Study:

  • To investigate the effects of exercise training on left ventricular remodeling in female spontaneously hypertensive rats (SHRs).
  • To examine cardiomyocyte hypertrophy, apoptosis, and proliferation in response to exercise in the context of hypertension.

Main Methods:

  • Four-month-old female SHRs underwent 12 weeks of treadmill exercise (SHR-TRD) or remained sedentary (SHR-SED).
  • Age-matched Wistar Kyoto (WKY) rats served as controls.
  • Cardiac structure, cardiomyocyte dimensions, apoptosis, proliferation markers, and specific protein/gene expression (calcineurin, Akt) were analyzed.

Main Results:

  • Exercise training (SHR-TRD) increased heart weight and left ventricular wall thickness compared to sedentary hypertensive rats (SHR-SED) and controls (WKY).
  • Cardiomyocyte hypertrophy (size) was augmented by exercise in hypertensive rats.
  • Apoptosis rate was increased in SHR-SED but mitigated by exercise in SHR-TRD.
  • Calcineurin abundance was attenuated by exercise, while cardiac progenitor cell (c-Kit+) abundance increased.

Conclusions:

  • Exercise training superimposed on established hypertension augments cardiomyocyte hypertrophy but attenuates calcineurin signaling.
  • Exercise mitigates apoptosis and tends to increase cardiac progenitor cells in hypertensive hearts.
  • Overall, exercise training may lead to a more favorable cardiomyocyte profile in hypertensive hearts.