Caroni P, Carafoli E
Proc Natl Acad Sci U S A. 1982 Oct;79(19):5763-7. doi: 10.1073/pnas.79.19.5763.
The movement of K+ in heart sarcolemmal vesicles has been followed through the opposing movement of the tetraphenylphosphonium ion. Ca2+ (5-50 microM) stimulates the efflux of K+ from K+-loaded vesicles [Km(Ca2+) approximately equal to 10 microM]. and the activation requires that Ca2+ be present inside the vesicles together with K+. The efflux of 86Rb+ from K+-, Rb+-loaded vesicles is similarly stimulated by 5-50 microM Ca2+ [Km(Ca2+) approximately equal to 10 microM]. The Ca2+-induced increase of K+ permeability does not become spontaneously inactivated. The effects of some inhibitors have been tested under conditions in which Ca2+ promotes the entry of K+ into vesicles. In this system, direct interaction of the drug with the Ca2+ and K+ membrane binding site(s) was therefore studied. Tetraethylammonium ion, which inhibits the potential-dependent K+ channel, does not interfere with the effect of Ca2+ whereas quinidine (IC50 = 12 microM) and trifluoperazine (IC50 = 8 microM at 50 micrograms of sarcolemmal protein per ml) inhibit.
通过四苯基鏻离子的反向移动来追踪心脏肌膜囊泡中K+的移动。Ca2+（5 - 50微摩尔）刺激K+负载囊泡中K+的外流[Km（Ca2+）约等于10微摩尔]，并且这种激活要求Ca2+与K+一起存在于囊泡内部。5 - 50微摩尔的Ca2+同样刺激K+、Rb+负载囊泡中86Rb+的外流[Km（Ca2+）约等于10微摩尔]。Ca2+诱导的K+通透性增加不会自发失活。在Ca2+促进K+进入囊泡的条件下测试了一些抑制剂的作用。因此，在这个系统中研究了药物与Ca2+和K+膜结合位点的直接相互作用。抑制电压依赖性K+通道的四乙铵离子不干扰Ca2+的作用，而奎尼丁（IC50 = 12微摩尔）和三氟拉嗪（每毫升50微克肌膜蛋白时IC50 = 8微摩尔）则有抑制作用。
