Goto A, Yamada K, Ishii M, Yoshioka M, Ishiguro T, Eguchi C, Sugimoto T
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
J Hypertens Suppl. 1988 Dec;6(4):S287-9. doi: 10.1097/00004872-198812040-00088.
We purified a polar digitalis-like factor to apparent homogeneity from human urine using inhibition of 3H-ouabain binding to intact human erythrocytes to monitor digitalis-like activity. Since endogenous digitalis-like factor may act as a natriuretic hormone, we tested the binding characteristics of this urine-derived ouabain-displacing compound to the sodium pump in intact renal epithelial cells, in order to assess its potential physiological significance. Cultured canine and porcine epithelial cell lines, MDCK and LLC-PK1, had a high sodium pump density as estimated from 3H-ouabain binding sites. Human urine-derived ouabain-displacing compound showed a dose-related inhibition of 3H-ouabain binding to both of these cells, similar to the inhibition of unlabelled ouabain. These findings indicate that the ouabain-displacing compound is capable of acting on the sodium pump in intact renal epithelial cells and may be the circulating regulator of Na+,K+-ATPase.
我们利用抑制³H-哇巴因与完整人红细胞的结合来监测洋地黄样活性，从人尿中纯化出一种极性洋地黄样因子，使其达到表观均一性。由于内源性洋地黄样因子可能作为一种利钠激素，我们测试了这种源自尿液的哇巴因置换化合物与完整肾上皮细胞中钠泵的结合特性，以评估其潜在的生理意义。从³H-哇巴因结合位点估计，培养的犬和猪上皮细胞系MDCK和LLC-PK1具有较高的钠泵密度。源自人尿的哇巴因置换化合物对这两种细胞的³H-哇巴因结合均表现出剂量相关的抑制作用，类似于未标记哇巴因的抑制作用。这些发现表明，哇巴因置换化合物能够作用于完整肾上皮细胞中的钠泵，可能是Na⁺,K⁺-ATP酶的循环调节因子。
