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Calmodulin abolishes the changes in Ca2+ binding and transport by heart sarcolemmal membranes of spontaneously

M David-Dufilho, M A Devynck

    Life Sciences
    |June 24, 1985
    PubMed

    Insights

    Calmodulin influences calcium handling in rat heart membranes. It enhances calcium binding and transport at physiological levels, normalizing differences between hypertensive and normotensive rats.

    Area of Science:

    • Cardiovascular Physiology
    • Molecular Cardiology
    • Biochemistry

    Background:

    • Spontaneously hypertensive rats (SHR) exhibit altered cardiac sarcolemmal Ca2+ transport and binding compared to normotensive WKY rats.
    • Calmodulin's role in regulating these Ca2+ handling processes at physiological intracellular calcium concentrations is not fully understood.

    Purpose of the Study:

    • To investigate the effects of calmodulin on Ca2+ binding and ATP-dependent Ca2+ transport in heart sarcolemmal membranes from SHR and WKY rats.
    • To determine if calmodulin can modulate the observed differences in Ca2+ handling between SHR and WKY rats.

    Main Methods:

    • Isolation of heart sarcolemmal membranes from spontaneously hypertensive rats (SHR) and normotensive WKY rats.
    • Measurement of Ca2+ binding and ATP-dependent Ca2+ accumulation by sarcolemmal membranes at varying free calcium concentrations (2.10(-8)M and 4.10(-7)M) in the presence and absence of calmodulin.

    Main Results:

    • At 2.10(-8)M free calcium, calmodulin did not significantly alter Ca2+ binding or ATP-dependent accumulation in either rat strain.
    • At 4.10(-7)M free calcium, calmodulin enhanced Ca2+ binding to SHR membranes and ATP-dependent Ca2+ transport in both SHR and WKY membranes.
    • Calmodulin presence suppressed the differences in Ca2+ binding and ATP-dependent accumulation between SHR and WKY membranes at 4.10(-7)M free calcium.

    Conclusions:

    • Calmodulin modulates Ca2+ handling in cardiac sarcolemmal membranes, particularly at higher physiological calcium concentrations.
    • Altered calmodulin content or function may contribute to the abnormal Ca2+ handling observed in the cardiac plasma membranes of SHR.

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