Kermode H, Chan W M, Williams A J, Sitsapesan R
Cardiac Medicine, NHLI, Imperial College School of Medicine, London, UK.
FEBS Lett. 1998 Jul 10;431(1):59-62. doi: 10.1016/s0014-5793(98)00725-x.
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.
在心肌缺血和再灌注期间,糖酵解活性增强,这可能导致糖酵解中间产物水平波动。我们证明,糖酵解的磷酸糖中间产物,特别是果糖-1,6-二磷酸(FDP;100微摩尔/升至10毫摩尔/升),可激活整合到双层膜中的绵羊心脏雷诺丁受体(RyR)通道(开放概率(Po)增加至约0.6),并刺激[3H]雷诺丁与分离的心肌肌浆网(SR)膜囊泡的结合(>200%)。磷酸糖在刺激[3H]雷诺丁结合和增加通道Po方面的相对有效性为FDP>葡萄糖-1-磷酸(G-1-P)>果糖-6-磷酸(F-6-P)>葡萄糖-6-磷酸(G-6-P)。磷酸糖化合物的这些新特性表明,糖酵解通量的变化可能通过调节RyR通道门控来影响SR Ca2+的释放。