Song Hong, Karashima Eiji, Hamlyn John M, Blaustein Mordecai P
Department of Physiology, University of Maryland School of Medicine, 655 W. Baltimore Street, Baltimore, MD 21201, USA.
J Physiol. 2014 Mar 1;592(5):941-69. doi: 10.1113/jphysiol.2013.266866. Epub 2013 Dec 16.
'Classic' cardiotonic steroids (CTSs) such as digoxin and ouabain selectively inhibit Na+, K+ -ATPase (the Na+ pump) and, via Na+ / Ca2+ exchange (NCX), exert cardiotonic and vasotonic effects. CTS action is more complex than previously thought: prolonged subcutaneous administration of ouabain, but not digoxin, induces hypertension, and digoxin antagonizes ouabain's hypertensinogenic effect. We studied the acute interactions between CTSs in two indirect assays of Na+ pump function: myogenic tone (MT) in isolated, pressurized rat mesenteric small arteries, and Ca2+ signalling in primary cultured rat hippocampal neurones. The 'classic' CTSs (0.3-10 nm) behaved as 'agonists': all increased MT70 (MT at 70 mmHg) and augmented glutamate-evoked Ca2+ (Fura-2) signals. We then tested one CTS in the presence of another. Most CTSs could be divided into ouabain-like (ouabagenin, dihydroouabain (DHO), strophanthidin) or digoxin-like CTS (digoxigenin, digitoxin, bufalin). Within each group, the CTSs were synergistic, but ouabain-like and digoxin-like CTSs antagonized one another in both assays: For example, the ouabain-evoked (3 nm) increases in MT70 and neuronal Ca2+ signals were both greatly attenuated by the addition of 10 nm digoxin or 10 nm bufalin, and vice versa. Rostafuroxin (PST2238), a digoxigenin derivative that displaces 3H-ouabain from Na+, K+ -ATPase, and attenuates some forms of hypertension, antagonized the effects of ouabain, but not digoxin. SEA0400, a Na+ / Ca2+ exchanger (NCX) blocker, antagonized the effects of both ouabain and digoxin. CTSs bind to the α subunit of pump αβ protomers. Analysis of potential models suggests that, in vivo, Na+ pumps function as tetraprotomers ((αβ)4) in which the binding of a single CTS to one protomer blocks all pumping activity. The paradoxical ability of digoxin-like CTSs to reactivate the ouabain-inhibited complex can be explained by de-oligomerization of the tetrameric state. The interactions between these common CTSs may be of considerable therapeutic relevance.
洋地黄毒苷和哇巴因等“经典”强心甾体(CTS)可选择性抑制钠钾ATP酶(钠泵),并通过钠钙交换(NCX)发挥强心和血管收缩作用。CTS的作用比之前认为的更为复杂:长期皮下注射哇巴因(而非洋地黄毒苷)会导致高血压,而洋地黄毒苷可拮抗哇巴因的致高血压作用。我们在钠泵功能的两种间接检测方法中研究了CTS之间的急性相互作用:分离的加压大鼠肠系膜小动脉中的肌源性张力(MT),以及原代培养的大鼠海马神经元中的钙信号传导。“经典”CTS(0.3 - 10纳米)表现为“激动剂”:均增加MT70(70毫米汞柱时的MT)并增强谷氨酸诱发的钙(Fura - 2)信号。然后我们在另一种CTS存在的情况下测试了一种CTS。大多数CTS可分为哇巴因样(哇巴因苷元、二氢哇巴因(DHO)、毒毛旋花子苷元)或洋地黄毒苷样CTS(地高辛苷元、洋地黄毒苷、蟾毒灵)。在每组中,CTS具有协同作用,但哇巴因样和洋地黄毒苷样CTS在两种检测中相互拮抗:例如,添加10纳米洋地黄毒苷或10纳米蟾毒灵会大大减弱哇巴因诱发的(3纳米)MT70增加和神经元钙信号增加,反之亦然。罗斯他福辛(PST2238)是一种地高辛苷元衍生物,可从钠钾ATP酶上置换3H - 哇巴因,并减轻某些形式的高血压,它可拮抗哇巴因的作用,但不能拮抗洋地黄毒苷的作用。SEA0400是一种钠钙交换体(NCX)阻滞剂,可拮抗哇巴因和洋地黄毒苷的作用。CTS与泵αβ原聚体的α亚基结合。对潜在模型的分析表明,在体内,钠泵以四聚体((αβ)4)形式发挥作用,其中单个CTS与一个原聚体的结合会阻断所有泵浦活性。洋地黄毒苷样CTS使哇巴因抑制的复合物重新激活这一看似矛盾的能力可通过四聚体状态的解聚来解释。这些常见CTS之间的相互作用可能具有相当大的治疗相关性。