Wolska B M, Lewartowski B
Department of Clinical Physiology, Medical Center of Postgraduate Education, Warsaw, Poland.
J Mol Cell Cardiol. 1993 Jan;25(1):75-91. doi: 10.1006/jmcc.1993.1009.
Inhibition of the Na-Ca exchange at the beginning of rest in isolated myocytes of the guinea-pig heart by means of superfusion with Na,Ca-free solution or 5.0 mM Ni2+ resulted in appearance of multiple phasic contractures. Contractures could not be initiated when the sarcoplasmic reticulum (SR) Ca2+ had been depleted by short (1 s) or steady state exposure to 10 mM caffeine, 0.1 microM ryanodine or due to rapid spontaneous release of the SR Ca2+ occurring sometimes at the beginning of rest. Superfusion with 2 x 10(-7) M thapsigargin, which blocked the SR Ca2+ uptake, prevented contractures otherwise initiated by superfusion with the Na,Ca-free solution. The frequency of spontaneous contractures was positively related to the rate of stimulation before rest and negatively related to the duration of rest before superfusion with the Na,Ca-free solution. It is proposed that in guinea-pig myocardium Ca2+ taken up by the SR from sarcoplasm or other cellular compartments like mitochondria, is released during diastole and rest to the subsarcolemmal space from which it is extruded by means of Na-Ca exchange. The release is a primary event not dependent on decrease of the resting sarcoplasmic free [Ca2+] by the outward Ca2+ transport. Inhibition of the Na-Ca exchange at the beginning of rest did not initiate any contractile response in rat myocytes. If the spontaneous contractures were already present, they were inhibited by superfusion with the Na,Ca-free solution. The result reflects the basic difference in the properties of SR of guinea-pig and rat.
用无钠、无钙溶液或5.0 mM Ni2+ 对豚鼠心脏分离的心肌细胞在静息开始时进行灌流，抑制钠钙交换会导致出现多次阶段性挛缩。当肌浆网（SR）的Ca2+ 通过短时间（1秒）或稳态暴露于10 mM咖啡因、0.1 μM 雷诺丁而耗尽，或者由于有时在静息开始时发生的SR Ca2+ 的快速自发释放时，挛缩无法启动。用2×10(-7) M毒胡萝卜素灌流，它阻断了SR对Ca2+ 的摄取，可防止因用无钠、无钙溶液灌流而引发的挛缩。自发挛缩的频率与静息前的刺激速率呈正相关，与用无钠、无钙溶液灌流前的静息持续时间呈负相关。有人提出，在豚鼠心肌中，SR从肌浆或其他细胞区室（如线粒体）摄取的Ca2+ 在舒张期和静息期释放到肌膜下空间，然后通过钠钙交换从该空间挤出。这种释放是一个主要事件，不依赖于通过外向Ca2+ 转运使静息肌浆游离[Ca2+] 降低。在静息开始时抑制钠钙交换在大鼠心肌细胞中不会引发任何收缩反应。如果已经存在自发挛缩，它们会因用无钠、无钙溶液灌流而受到抑制。该结果反映了豚鼠和大鼠SR特性的基本差异。
