Cloix J F, Crabos M, Grichois M L, Meyer P
Département de pharmacologie, INSERM U7 CNRS UA318, Hôpital Necker, Paris, France.
Can J Physiol Pharmacol. 1987 Aug;65(8):1522-7. doi: 10.1139/y87-240.
Plasma and urine levels of an endogenous digitalis-like compound (EDLC) are increased in low renin Na+-dependent experimental hypertension, in some normotensive offspring of hypertensive patients and in some essential hypertensive patients. Urine-drived EDLC was purified from 550 L of urine from essential hypertensive patients (n = 8) and from normotensive subjects with a family history of hypertension (n = 27), using flash chromatography on C18 reversed-phase, anion exchange chromatography and various reversed-phase high performance liquid chromatographies. The mechanism of Na+-K+ ATPase inhibition and the related effects of semipurified urine-derived EDLC were studied and compared with those of ouabain. Its action was similar to that of ouabain in 8 out of 10 of the tests applied. The main effects of such a compound were the depression of Na+-K+ pump activity of human erythrocytes, the inhibition of 5-hydroxytryptamine reuptake by human platelets, and the induction of natriuresis in urethanized rats. Therefore, EDLC may be considered as one of the natriuretic hormones whose mechanism of action closely resembles that of ouabain.
在低肾素钠依赖性实验性高血压患者、部分高血压患者的血压正常的后代以及部分原发性高血压患者中，内源性洋地黄样化合物（EDLC）的血浆和尿液水平会升高。使用C18反相快速色谱法、阴离子交换色谱法和各种反相高效液相色谱法，从8例原发性高血压患者和27例有高血压家族史的血压正常受试者的550升尿液中纯化出尿源性EDLC。研究了Na+-K+ ATP酶抑制机制以及半纯化尿源性EDLC的相关作用，并与哇巴因进行了比较。在所应用的10项测试中，有8项测试显示其作用与哇巴因相似。这种化合物的主要作用包括抑制人红细胞的Na+-K+泵活性、抑制人血小板对5-羟色胺的再摄取以及诱导乌拉坦麻醉大鼠的利钠作用。因此，EDLC可被视为一种利钠激素，其作用机制与哇巴因极为相似。
