Ozaki H, Nagase H, Urakawa N
J Pharmacol Exp Ther. 1984 Oct;231(1):153-8.
The effects of ouabain and other cardiotonic steroids were examined to investigate whether changes in Na,K-adenosine triphosphatase (ATPase) activity modified the actions of palytoxin (PTX) in rabbit aortic vascular smooth muscle. The effects of these agents on rabbit aorta were compared with those on rat aorta, as it is known that the concentration of cardiac glycosides required to inhibit Na,K-ATPase of rat aorta is markedly higher than that of other species. PTX induced contraction in rabbit and rat aortas in a similar concentration range (10(-11) to 10(-8) M). PTX rapidly decreased tissue K content of these preparations. Ouabain (2 X 10(-5) M) inhibited both the contraction and the loss of tissue K in rabbit aorta but not in rat aorta. In rabbit aorta, convallatoxin (2 X 10(-5) M), which has one rhamnose as a sugar moiety like ouabain, and cymarin (2 X 10(-5) M), which has one cymarose, inhibited the PTX-induced contraction and the loss of tissue K, although ouabagenin, convallatoxigenin and cymarigenin (strophanthidin) (2 X 10(-5) M) did not. Other cardiotonic steroids, digoxin and digitoxin, which have 3 U of digitoxose as a sugar component, or the corresponding aglycones failed to inhibit the PTX-responses. On the other hand, all the cardiotonic steroids at concentration of 2 X 10(-5) M equally inhibited the reuptake of K and relaxation of norepinephrine-induced contractions induced by the readdition of K. Inhibition of Na-K pump by K-free solution potentiated rather than inhibited the PTX-induced contraction. These results suggest that the specific sugar moiety of cardiac glycosides is important for the inhibitory effect exerted by these compounds on the PTX-induced responses and that the inhibition is not related to the activity of the Na,K-ATPase.
研究哇巴因及其他强心甾体的作用，以探讨钠钾 - 三磷酸腺苷酶（ATP酶）活性的变化是否会改变兔主动脉血管平滑肌中短裸甲藻毒素（PTX）的作用。将这些药物对兔主动脉的作用与对大鼠主动脉的作用进行比较，因为已知抑制大鼠主动脉钠钾ATP酶所需的强心苷浓度明显高于其他物种。PTX在相似的浓度范围（10⁻¹¹至10⁻⁸M）内诱导兔和大鼠主动脉收缩。PTX迅速降低这些标本的组织钾含量。哇巴因（2×10⁻⁵M）抑制兔主动脉的收缩和组织钾的丢失，但不抑制大鼠主动脉的。在兔主动脉中，与哇巴因一样具有一个鼠李糖作为糖部分的铃兰毒苷（2×10⁻⁵M）和具有一个洋地黄糖的洋地黄毒苷（2×10⁻⁵M）抑制PTX诱导的收缩和组织钾的丢失，尽管哇巴因苷元、铃兰毒苷元和洋地黄毒苷元（毒毛旋花子苷元）（2×10⁻⁵M）没有。其他强心甾体，具有3个洋地黄毒糖作为糖成分的地高辛和洋地黄毒苷，或相应的苷元未能抑制PTX反应。另一方面，所有浓度为2×10⁻⁵M的强心甾体均同等程度地抑制钾的再摄取以及由再添加钾诱导的去甲肾上腺素诱导的收缩的松弛。无钾溶液对钠钾泵的抑制增强而非抑制PTX诱导的收缩。这些结果表明，强心苷的特定糖部分对于这些化合物对PTX诱导反应的抑制作用很重要，并且这种抑制与钠钾ATP酶的活性无关。
