机制引起的高钾血症nafamostat甲磺酸盐:影响的两个代谢物Na +和K +交通属性在兔子皮质集合管。

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Muto年代,Imai M,浅野Y

机制引起的高钾血症nafamostat甲磺酸盐:影响的两个代谢物Na +和K +交通属性在兔子皮质集合管。

Br J杂志。1994年1月,111 (1):173 - 8。

PubMed ID

8012693 (在PubMed

]

文摘

1。目前的实验进行确定造成高钾血症的机制(s) nafamostat甲磺酸盐(NM),一种丝氨酸蛋白酶抑制剂。2。我们调查的影响,腔的两种代谢物的海里,p-guanidinobenzoic酸(PGBA)和6-amidino-2-naphthol(一个),在Na +和K +运输的属性集尿管(CD)的细胞包括皮质集合管(CCD)从兔肾脏,因为这些代谢物,但不是海里,主要是分泌到尿液。3所示。添加PGBA 10(5)和10 (4)M腔导致超极化的VA与增加transepithelial阻力(RT)和部分顶端膜电阻(fRA)。PGBA添加到腔内灌注液10(5)和10 (4)M改变了弗吉尼亚州,RT和联邦铁路局剂量依赖性的方式。这些影响是完全被预处理与腔的阿米洛利(50 microM)。PGBA在10(6)米腔对电气参数没有影响。4所示。 Luminal addition of AN at 10(-4) M also caused the apical membrane to hyperpolarize in parallel with increases in RT and fRA. These effects were also completely inhibited by pretreatment with luminal amiloride (50 microM). AN at 10(-5) M in the lumen had no effect on the electrical parameters. 5. We conclude that two metabolites of NM, PGBA and AN, act on the apical membrane of the CD cell and inhibit the amiloride-sensitive Na+ conductance, resulting in an inhibition of K+ secretion. This direct action of these metabolites, rather than NM, on the CCD might contribute to the NM-induced hyperkalaemia.

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药物

Nafamostat