Sutko J L, Bers D M, Reeves J P
Am J Physiol. 1986 Apr;250(4 Pt 2):H654-61. doi: 10.1152/ajpheart.1986.250.4.H654.
To determine whether Na+-Ca2+ exchange is a physiologically significant Ca2+ efflux mechanism in rabbit ventricle, we investigated the effects exerted on postrest contractions by interventions that alter the transmembrane distribution of Na+ or Ca2+ so as to retard Ca2+ efflux via this system. Contractions elicited after rest periods of 0.25-10 min in duration were studied. The following interventions increased postrest contractions much more than those elicited by rhythmic stimulation: 1) Na+ pump inhibition by cardiac glycosides or by a reduction in extracellular K+, 2) reduction of extracellular Na+ (maintaining a constant [Ca2+]-to-[Na+]2 ratio), and 3) elevation of extracellular Ca2+. In contrast, isoproterenol, norepinephrine, and histamine produced comparable increases in both rhythmically stimulated and postrest contractions, suggesting that the postrest contractile potentiation was not just the result of a general increase in inotropic state. Ryanodine, which appears to antagonize sarcoplasmic reticulum (SR) Ca2+ release in cardiac muscle, markedly reduced the amplitude of the postrest contractions, but only modestly decreased rhythmically stimulated responses. Results suggest 1) that Ca2+ released from SR is involved in postrest response, 2) that Na+-Ca2+ exchange serves as a Ca2+ efflux pathway in normally polarized resting rabbit ventricle, and 3) that this activity in part determines the amount of Ca2+ available for release from SR.
为了确定钠钙交换是否是兔心室中一种具有生理意义的钙外流机制，我们研究了改变钠或钙的跨膜分布以减缓通过该系统的钙外流的干预措施对静息后收缩的影响。研究了持续时间为0.25 - 10分钟的静息期后引发的收缩。以下干预措施对静息后收缩的增强作用远大于节律性刺激引发的收缩：1）强心苷或细胞外钾减少对钠泵的抑制；2）细胞外钠减少（保持恒定的[钙]与[钠]²比值）；3）细胞外钙升高。相比之下，异丙肾上腺素、去甲肾上腺素和组胺在节律性刺激和静息后收缩中产生的增加作用相当，这表明静息后收缩增强不仅仅是心肌收缩力普遍增加的结果。似乎能拮抗心肌肌浆网（SR）钙释放的ryanodine显著降低了静息后收缩的幅度，但仅适度降低了节律性刺激反应。结果表明：1）从SR释放的钙参与静息后反应；2）钠钙交换在正常极化的静息兔心室中作为钙外流途径；3）这种活性部分决定了可从SR释放的钙量。
