The authors propose using electron probe microanalysis to directly demonstrate calcium release from the junctional sarcoplasmic reticulum during cardiac muscle contraction.
May enable direct study of SR calcium release in animal hearts; leaves open validation and translation to human cardiac physiology.
Substantial evidence suggests that the increase in cytosolic Ca 2+ which occurs upon stimulation of cardiac muscle originates from the sarcoplasmic reticulum (SR) and that its release is triggered by a transient rise in cytosolic Ca 2+ . The junctional SR has been proposed as a Ca 2+ release site, based on a number of observations, e.g. measurements by EPMA have demonstrated significant Ca 2+ stores in the junctional SR in resting cardiac muscle; the ryanodine-sensitive Ca 2+ release channels are associated with junctional SR membrane and the low affinity Ca 2+ binding protein, calsequestrin, is localized to the junctional SR. Although considerable evidence implicates the junctional SR as an intracellular Ca 2+ store in cardiac muscle, release of Ca 2+ from the junctional SR, upon muscle stimulation, has not been directly demonstrated. We therefore propose to use EPMA to directly measure the Ca 2+ content of junctional SR in both relaxed and contracted cardiac muscle to determine whether Ca 2+ is released from the junctional SR during contraction.
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Moravec et al. (1990) studied this question.
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