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Updated: Aug 19, 2026

Optical Mapping of Intra-Sarcoplasmic Reticulum Ca2+ and Transmembrane Potential in the Langendorff-perfused Rabbit Heart
09:26

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

Published on: September 10, 2015

Ca-releasing action of beta, gamma-methylene adenosine triphosphate on fragmented sarcoplasmic reticulum

Y Ogawa, S Ebashi

    Journal of Biochemistry
    |November 1, 1976
    PubMed

    Insights

    beta,gamma-Methylene adenosine triphosphate (AMPOPCP) inhibits calcium uptake and triggers calcium release from fragmented sarcoplasmic reticulum (FSR). Its action on FSR suggests the complex

    Area of Science:

    • * Biochemistry and molecular biology of calcium handling in muscle cells.
    • * Sarcoplasmic reticulum (SR) function and calcium regulation.
    • * Adenosine triphosphate (ATP) analog mechanisms.

    Background:

    • * Fragmented sarcoplasmic reticulum (FSR) plays a critical role in muscle contraction and relaxation by regulating intracellular calcium (Ca) levels.
    • * Calcium uptake and release by the SR are essential processes modulated by various factors and molecules.
    • * Understanding the precise mechanisms of Ca release is vital for comprehending muscle physiology and pathology.

    Purpose of the Study:

    • * To investigate the effects of beta,gamma-Methylene adenosine triphosphate (AMPOPCP) on calcium handling by fragmented sarcoplasmic reticulum (FSR).
    • * To elucidate the mechanism by which AMPOPCP induces calcium release and compare it to calcium-induced calcium release (CICR).
    • * To determine the role of the FSR-ATP complex state in mediating calcium release.

    Main Methods:

    • * Experiments involving fragmented sarcoplasmic reticulum (FSR) isolated from muscle tissue.
    • * Measurement of Ca uptake rates and Ca release induced by AMPOPCP.
    • * Assessment of the effects of procaine, varying Ca concentrations, and Mg concentrations on AMPOPCP-induced Ca release.
    • * Investigation of the potentiation of AMPOPCP's action by caffeine.
    • * Analysis of the phosphorylated intermediate (EP) and Sr release.

    Main Results:

    • * AMPOPCP was found to inhibit the rate of Ca uptake into FSR.
    • * AMPOPCP induced Ca release from Ca-loaded FSR, sharing characteristics with CICR, including inhibition by procaine and facilitation by increased Ca concentration.
    • * Ca release was not facilitated by decreased Mg concentration.
    • * AMPOPCP and caffeine exhibited a remarkable synergistic effect on Ca release.
    • * The state of the FSR-ATP complex was implicated in Ca-induced Ca release.

    Conclusions:

    • * AMPOPCP exhibits dual effects on FSR: inhibiting Ca uptake and inducing Ca release.
    • * The Ca release induced by AMPOPCP shares significant mechanistic similarities with calcium-induced calcium release.
    • * The findings suggest that the phosphorylation state of the FSR-ATP complex is a critical determinant for calcium-induced calcium release.

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