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Updated: Nov 16, 2025

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

Published on: April 30, 2020

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Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload

I F S Mazeto1, K Okoshi2, C F S M P Silveira2

  • 1Departamento de Infectologia, Dermatologia, Diagnóstico por Imagem e Radioterapia, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista, Botucatu, SP, Brasil.

Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas
|February 24, 2021
PubMed

Insights

Pressure overload from aortic stenosis impairs heart function by altering calcium handling proteins, specifically decreasing Na+/Ca2+ exchanger (NCX1) and SERCA2a, leading to diastolic dysfunction.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Physiology

Background:

  • Cardiac calcium (Ca2+) homeostasis is crucial for heart function.
  • Sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) and sarcolemmal Na+/Ca2+ exchanger (NCX1) are key regulators of Ca2+ handling.
  • Previous research indicates altered SERCA2a and NCX1 function in heart failure.

Purpose of the Study:

  • To investigate the impact of pressure overload on heart function.
  • To evaluate the behavior of Ca2+-handling proteins in hypertrophied heart muscle.
  • To assess changes in SERCA2a and NCX1 under pressure overload conditions.

Main Methods:

  • Aortic stenosis (AoS) model in Wistar rats (n=20) compared to Sham controls.
  • Echocardiography for cardiac function and structure assessment.
  • Isolated papillary muscle (IPM) analysis for myocardial function and Ca2+ handling.
  • Western blot (WB) for Ca2+-handling protein expression (NCX1, SERCA2a, PLB).

Main Results:

  • AoS induced concentric hypertrophy with preserved ejection fraction but diastolic dysfunction (dilated left atrium, increased wall thickness).
  • IPM studies revealed increased resting tension (stiffness) and altered Ca2+ handling in AoS rats.
  • WB showed decreased expression of NCX1, SERCA2a, and phosphorylated phospholambam (PLB) on serine-16 in the AoS group.

Conclusions:

  • Aortic stenosis leads to left ventricular hypertrophy and diastolic dysfunction.
  • Impaired cardiac function in AoS is associated with deficits in NCX1, SERCA2a, and phosphorylated PLB.
  • These findings highlight the critical role of Ca2+ handling protein dysregulation in pressure-induced heart disease.

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