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Related Experiment Videos

Impaired sarcoplasmic reticulum function leads to contractile dysfunction and cardiac hypertrophy.

M Meyer1, S U Trost, W F Bluhm

  • 1Department of Medicine, University of California, San Diego, California 92093, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|April 12, 2001
PubMed
Summary

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Targeting sarcoplasmic reticulum (SR) function impairs cardiac contractility and relaxation. This leads to cardiac hypertrophy and altered gene expression, suggesting SR dysfunction can initiate heart problems.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Physiology

Background:

  • Sarcoplasmic reticulum (SR) Ca(2+) handling is crucial for cardiac contractility.
  • SR dysfunction is implicated in heart failure.
  • The direct causal link between SR dysfunction and cardiac remodeling is not fully understood.

Purpose of the Study:

  • To investigate if targeted SR dysfunction can independently cause cardiac contractile impairment.
  • To determine if SR dysfunction alters cardiac gene expression and induces hypertrophy.
  • To establish a novel animal model for studying SR-mediated cardiac dysfunction.

Main Methods:

  • Developed a mouse model by administering ryanodine in drinking water to interfere with SR Ca(2+) release.
  • Performed in vivo hemodynamic measurements to assess cardiac contractility and relaxation.

Related Experiment Videos

  • Analyzed cardiac hypertrophy and gene expression changes (atrial natriuretic factor, beta-myosin heavy chain, SR Ca(2+)) after 1 and 4 weeks of treatment.

    • Main Results:

    • Ryanodine treatment reduced maximal contraction speed (+dP/dt(max)) by 28% and relaxation speed (-dP/dt(max)) by 24% after 1 week.
    • Cardiac relaxation was significantly slowed, with the late phase prolonged by 22%.
    • After 4 weeks, significant cardiac hypertrophy was observed, particularly in the atria, accompanied by increased expression of stress-response genes and reduced SR Ca(2+) mRNA.

    Conclusions:

    • Selective impairment of SR function in vivo can be a primary cause of cardiac contractile dysfunction.
    • SR dysfunction can induce cardiac hypertrophy and alter cardiac gene expression profiles.
    • This study provides evidence that SR dysfunction can initiate pathological cardiac remodeling.