Sugar phosphate intermediates of glycolysis can activate cardiac ryanodine receptors, indicating a mechanism by which glycolytic flux changes during ischemia/reperfusion may modulate SR calcium release.
May link glycolytic intermediates to RyR gating in ischemia; hypothesis-generating in animals and leaves open human relevance.
During myocardial ischaemia and reperfusion, enhancement of glycolytic activity occurs and this may lead to fluctuating levels of glycolytic intermediates. We demonstrate that sugar phosphate intermediates of glycolysis, particularly fructose-1,6-diphosphate (FDP; 100 microM-10 mM), can activate sheep cardiac ryanodine receptor (RyR) channels incorporated into bilayers (open probability (Po) increases up to approximately 0.6) and stimulate [3H]ryanodine binding (> 200%) to isolated cardiac sarcoplasmic reticulum (SR) membrane vesicles. The relative effectiveness of the sugar phosphates in stimulating [3H]ryanodine binding and increasing the Po of the channels was FDP > glucose-1-phosphate (G-1-P) > fructose-6-phosphate (F-6-P) > glucose-6-phosphate (G-6-P). These novel properties of the sugar phosphate compounds indicate that changes in glycolytic flux may influence the release of SR Ca2+ by modulating RyR channel gating.
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Kermode et al. (1998) studied this question.
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