Soler A, Alda J O, Gimenez I, Garcia C, Nazaret C, Parés I, Garay R P
INSERM U2/CNRS UA 130251, Faculté de Médecine, Créteil, France.
Pflugers Arch. 1994 Feb;426(3-4):357-9. doi: 10.1007/BF00374795.
We previously found a potent inhibitor of the Na-K-Cl cotransport system in urines from salt-loaded rats (C.I.F. = cotransport inhibitory factor, ref. 1). Here we extracted an urinary fraction (approximately 1% urine dry weight), free from immunoreactive A.N.P. and digoxin activity, which: (i) potently inhibited cotransport fluxes in MDCK (Madin and Darby canine kidney] cells and in human erythrocytes, (ii) inhibited Na(+)-dependent chloride/bicarbonate exchange with 2-3 times less potency than cotransport and (iii) strongly increased natriuresis and diuresis after i.v. infusion in rats with no significant change in kaliuresis (salidiuretic action reduced by probenecid). Therefore, C.I.F. seems to be a new natriuretic factor with part, but not all the biological profile of loop diuretic drugs.
我们之前在盐负荷大鼠的尿液中发现了一种强效的钠 - 钾 - 氯共转运系统抑制剂（C.I.F. = 共转运抑制因子，参考文献1）。在此，我们从尿液中提取了一种组分（约占尿液干重的1%），该组分不含免疫反应性心钠素（A.N.P.）和地高辛活性，其具有以下特性：（i）能有效抑制MDCK（麦迪逊和达比犬肾）细胞及人红细胞中的共转运通量；（ii）抑制钠依赖性氯/碳酸氢根交换的效力比共转运低2 - 3倍；（iii）静脉注射到大鼠体内后，能显著增加尿钠排泄和利尿作用，而尿钾排泄无明显变化（丙磺舒可降低其促尿钠排泄作用）。因此，C.I.F.似乎是一种新的利钠因子，具有部分但并非全部袢利尿剂的生物学特性。
