Artigas Pablo, Gadsby David C
Laboratory of Cardiac/Membrane Physiology, Rockefeller University, New York, NY 10021-6399, USA.
J Gen Physiol. 2004 Apr;123(4):357-76. doi: 10.1085/jgp.200308964. Epub 2004 Mar 15.
Palytoxin binds to Na/K pumps to generate nonselective cation channels whose pore likely comprises at least part of the pump's ion translocation pathway. We systematically analyzed palytoxin's interactions with native human Na/K pumps in outside-out patches from HEK293 cells over a broad range of ionic and nucleotide conditions, and with or without cardiotonic steroids. With 5 mM internal (pipette) [MgATP], palytoxin activated the conductance with an apparent affinity that was highest for Na(+)-containing (K(+)-free) external and internal solutions, lowest for K(+)-containing (Na(+)-free) external and internal solutions, and intermediate for the mixed external Na(+)/internal K(+), and external K(+)/internal Na(+) conditions; with Na(+) solutions and MgATP, the mean dwell time of palytoxin on the Na/K pump was about one day. With Na(+) solutions, the apparent affinity for palytoxin action was low after equilibration of patches with nucleotide-free pipette solution. That apparent affinity was increased in two phases as the equilibrating [MgATP] was raised over the submicromolar, and submillimolar, ranges, but was increased by pipette MgAMPPNP in a single phase, over the submillimolar range; the apparent affinity at saturating [MgAMPPNP] remained approximately 30-fold lower than at saturating [MgATP]. After palytoxin washout, the conductance decay that reflects palytoxin unbinding was accelerated by cardiotonic steroid. When Na/K pumps were preincubated with cardiotonic steroid, subsequent activation of palytoxin-induced conductance was greatly slowed, even after washout of the cardiotonic steroid, but activation could still be accelerated by increasing palytoxin concentration. These results indicate that palytoxin and a cardiotonic steroid can simultaneously occupy the same Na/K pump, each destabilizing the other. The palytoxin-induced channels were permeable to several large organic cations, including N-methyl-d-glucamine(+), suggesting that the narrowest section of the pore must be approximately 7.5 A wide. Enhanced understanding of palytoxin action now allows its use for examining the structures and mechanisms of the gates that occlude/deocclude transported ions during the normal Na/K pump cycle.
刺尾鱼毒素与钠钾泵结合,生成非选择性阳离子通道,其孔道可能至少部分由泵的离子转运途径构成。我们系统地分析了刺尾鱼毒素在广泛的离子和核苷酸条件下,以及在有或无强心甾存在的情况下,与来自HEK293细胞的外向膜片中天然人类钠钾泵的相互作用。在内部(移液管)[MgATP]浓度为5 mM时,刺尾鱼毒素激活电导的表观亲和力在外部和内部溶液含Na⁺(无K⁺)时最高,在外部和内部溶液含K⁺(无Na⁺)时最低,在外部Na⁺/内部K⁺以及外部K⁺/内部Na⁺的混合条件下处于中间水平;在含Na⁺溶液和MgATP的情况下,刺尾鱼毒素在钠钾泵上的平均停留时间约为一天。在使用含Na⁺溶液时,用无核苷酸的移液管溶液平衡膜片后,刺尾鱼毒素作用的表观亲和力较低。随着平衡时的[MgATP]在亚微摩尔和亚毫摩尔范围内升高,表观亲和力分两个阶段增加,但在亚毫摩尔范围内,移液管中的MgAMPPNP以单相增加表观亲和力;在饱和[MgAMPPNP]时的表观亲和力仍比饱和[MgATP]时低约30倍。在洗去刺尾鱼毒素后,反映刺尾鱼毒素解离的电导衰减被强心甾加速。当钠钾泵与强心甾预孵育后,随后刺尾鱼毒素诱导的电导激活大大减慢,即使在洗去强心甾后也是如此,但增加刺尾鱼毒素浓度仍可加速激活。这些结果表明,刺尾鱼毒素和强心甾可同时占据同一个钠钾泵,二者相互使对方不稳定。刺尾鱼毒素诱导的通道对几种大的有机阳离子通透,包括N - 甲基 - D - 葡糖胺⁺,这表明孔道最窄部分的宽度必须约为7.5埃。对刺尾鱼毒素作用的进一步了解现在使其可用于研究在正常钠钾泵循环中阻塞/解除阻塞转运离子的门的结构和机制。