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Updated: May 5, 2026

Optical Mapping of Intra-Sarcoplasmic Reticulum Ca2+ and Transmembrane Potential in the Langendorff-perfused Rabbit Heart
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Optical Mapping of Intra-Sarcoplasmic Reticulum Ca2+ and Transmembrane Potential in the Langendorff-perfused Rabbit Heart

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Excitation-contraction coupling in heart. VII. Calcium accumulation in subcellular particles in congestive heart

P V Sulakhe, N S Dhalia

    The Journal of Clinical Investigation
    |May 1, 1971
    PubMed

    Insights

    Congestive heart failure in hamsters shows impaired calcium uptake by heart cell mitochondria and microsomes. This suggests a defective calcium pump may cause heart failure.

    Area of Science:

    • Cardiovascular Biology
    • Cellular Physiology
    • Biochemistry

    Background:

    • Congestive heart failure is a complex condition affecting heart muscle function.
    • Understanding subcellular mechanisms of calcium handling is crucial for identifying heart failure causes.

    Purpose of the Study:

    • To investigate calcium accumulation in heavy microsomes and mitochondria from control and failing hamster hearts.
    • To identify potential defects in calcium transport associated with heart failure.

    Main Methods:

    • Isolation of heavy microsomes and mitochondria from control and dystrophic hamster hearts (BIO 14.6 strain).
    • Measurement of energy-linked calcium binding and calcium uptake under various conditions (e.g., presence/absence of oxalate, Pi, succinate).
    • Assay of total adenosine triphosphatase activities.

    Main Results:

    • Energy-linked calcium binding by heavy microsomes was depressed in failing hearts, but oxalate-supported uptake was similar to controls.
    • Mitochondrial calcium binding and uptake were significantly reduced in failing hearts compared to controls.
    • No differences in total Ca(++)-Mg(++) stimulated adenosine triphosphatase activities were found.

    Conclusions:

    • Failing hamster hearts exhibit abnormalities in subcellular membrane calcium binding.
    • Results support the hypothesis of a defective calcium pump as a molecular abnormality in moderate congestive heart failure.

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