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水通道蛋白-1介导氯化钠诱导的水通过直小血管降支流动的证据。

Evidence that aquaporin-1 mediates NaCl-induced water flux across descending vasa recta.

作者信息

Pallone T L, Kishore B K, Nielsen S, Agre P, Knepper M A

机构信息

Division of Nephrology, University of School of Medicine, Baltimore 21201-1595, USA.

出版信息

Am J Physiol. 1997 May;272(5 Pt 2):F587-96. doi: 10.1152/ajprenal.1997.272.5.F587.

DOI:10.1152/ajprenal.1997.272.5.F587
PMID:9176368
Abstract

Outer medullary descending vasa recta (OMDVR) were perfused in vitro, and volume efflux was measured by driving water movement with transmural gradients of NaCl or albumin. Consistent with mediation by water channels, p-chloromercuribenzenesulfonic acid (pCMBS) markedly inhibited volume flux induced by NaCl. Dithiothreitol reversed the inhibition, pCMBS did not significantly alter water flux induced by albumin. Osmotic water permeability (Pf) of the pCMBS-sensitive pathway of glutaraldehyde-fixed and nonfixed OMDVR was 1,102 +/- 449 and 1,257 +/- 718 microns/s (means +/- SD), respectively. pCMBS reduced Pf to near zero, whereas diffusional water permeability in the same vessels was only slightly inhibited. Immunoreactive aquaporin-1 (AQP1) measured by enzyme-linked immunosorbent assay in collagenase-treated and untreated OMDVR was 5.2 +/- 1.0 and 4.2 +/- 0.4 fmol/mm, respectively, values that account well for the experimental Pf. We conclude that OMDVR water flux driven by NaCl gradients is most likely mediated by the AQP1 water channel and that NaCl and urea gradients drive water efflux in vivo by this route.

摘要

对肾外髓质降支直小血管(OMDVR)进行体外灌注,通过NaCl或白蛋白的跨壁梯度驱动水的流动来测量容积流出量。与水通道介导一致,对氯汞苯磺酸盐(pCMBS)显著抑制了NaCl诱导的容积通量。二硫苏糖醇可逆转这种抑制作用,pCMBS对白蛋白诱导的水通量没有显著影响。戊二醛固定和未固定的OMDVR的pCMBS敏感途径的渗透水通透性(Pf)分别为1102±449和1257±718微米/秒(平均值±标准差)。pCMBS将Pf降低至接近零,而同一血管中的扩散水通透性仅略有抑制。通过酶联免疫吸附测定法在胶原酶处理和未处理的OMDVR中测得的免疫反应性水通道蛋白-1(AQP1)分别为5.2±1.0和4.2±0.4飞摩尔/毫米,这些值很好地解释了实验测得的Pf。我们得出结论,由NaCl梯度驱动的OMDVR水通量很可能由AQP1水通道介导,并且NaCl和尿素梯度在体内通过该途径驱动水流出。

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