Mead R H, Clusin W T
Biophys J. 1985 Nov;48(5):695-700. doi: 10.1016/S0006-3495(85)83827-3.
Although lanthanum ions (La+++) block calcium influx in cardiac cells, they may paradoxically accentuate the sodium-free contracture. We have therefore studied the effects of La+++ on the zero sodium response in chick embryonic myocardial cell aggregates. Zero sodium alone causes: (a) A maintained contracture; (b) Asynchronous localized contractions that are selectively inhibited by caffeine or ryanodine, and presumably reflect release of calcium from the sarcoplasmic reticulum; (c) A nonspecific conductance increase that is ascribable to calcium-activated ion channels. Addition of La+++ potentiates the sodium-free contracture, and causes similar potentiation of the localized contractions and the conductance increase. All three phenomena occur 5-10-fold faster in 1 mM La+++ than in sodium-free fluid alone. In contrast, when La+++ is combined with caffeine or ryanodine, the zero sodium response is suppressed. We conclude that the paradoxical effect of La+++ on the contracture is not due to calcium influx, but to enhancement, or disinhibition of intracellular calcium release. Relaxation of normal myocardium may involve control of spontaneous calcium release by lanthanum- and sodium-sensitive calcium transport across the surface membrane.
尽管镧离子(La+++)可阻断心肌细胞中的钙内流,但它们可能反常地加剧无钠挛缩。因此,我们研究了La+++对鸡胚心肌细胞聚集体零钠反应的影响。仅零钠就会导致:(a)持续性挛缩;(b)咖啡因或ryanodine可选择性抑制的异步局部收缩,推测这反映了肌浆网中钙的释放;(c)归因于钙激活离子通道的非特异性电导增加。添加La+++会增强无钠挛缩,并使局部收缩和电导增加产生类似的增强作用。在1 mM La+++中,所有这三种现象出现的速度比仅在无钠溶液中快5至10倍。相反,当La+++与咖啡因或ryanodine联合使用时,零钠反应受到抑制。我们得出结论,La+++对挛缩的反常作用不是由于钙内流,而是由于细胞内钙释放的增强或去抑制。正常心肌的舒张可能涉及通过镧和钠敏感的钙跨表面膜转运来控制自发钙释放。