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Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes
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Cardiac contractile dysfunction in J2N-k cardiomyopathic hamsters is associated with impaired SR function and

Andrea P Babick1, Elliott J F Cantor, John T Babick

  • 1Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada R2H 2A6.

American Journal of Physiology. Cell Physiology
|July 2, 2004
PubMed

Insights

Dilated cardiomyopathy (DCM) in J2N-k hamsters impairs heart function by disrupting sarcoplasmic reticulum (SR) calcium handling. This leads to reduced SR calcium uptake, impacting cardiac contractility.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Physiology

Background:

  • Dilated cardiomyopathy (DCM) causes cardiac contractile dysfunction, but mechanisms remain unclear.
  • The sarcoplasmic reticulum (SR) regulates intracellular calcium (Ca2+), crucial for heart contraction and relaxation.

Purpose of the Study:

  • To investigate if SR function and regulation abnormalities contribute to cardiac contractile dysfunction in the J2N-k cardiomyopathic hamster model of DCM.

Main Methods:

  • Echocardiography to assess cardiac function (ejection fraction, fractional shortening, cardiac output, heart rate).
  • Measurement of cardiac SR Ca2+ uptake.
  • Analysis of SR Ca2+-ATPase expression and phospholamban (PLB) phosphorylation at serine-16.
  • Assay of SR-associated cAMP-dependent protein kinase (PKA) activity and protein phosphatase activity.

Main Results:

  • J2N-k hamsters exhibited significantly reduced ejection fraction, fractional shortening, cardiac output, and heart rate compared to controls.
  • Cardiac function depression correlated with decreased cardiac SR Ca2+ uptake.
  • Reduced SR Ca2+ uptake was linked to decreased SR Ca2+-ATPase expression and reduced PKA-mediated PLB phosphorylation.
  • Lower PLB phosphorylation coincided with reduced SR-associated PKA activity and elevated protein phosphatase activity.

Conclusions:

  • Alterations in SR function and its regulation contribute to cardiac contractile dysfunction in the J2N-k cardiomyopathic hamster.
  • Dysregulated calcium handling by the SR is a key factor in DCM pathogenesis in this model.

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