K-Cl transport systems in rabbit renal basolateral membrane vesicles.

K-Cl transport systems in rabbit renal basolateral membrane vesicles.
复制标题

兔肾基底外侧膜囊泡中的 K-Cl 转运系统。

DOI:
10.1152/ajprenal.1987.252.5.f883
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发表时间:
1987
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Warnock,DG
Warnock,DG
中科院分区:
--
文献类型:
--
作者:
Eveloff,J;Warnock,DG

文献摘要

被引文献

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研究了氯离子在兔肾皮质基底外侧膜囊中的转运途径。与钠或n -甲基- d -氨基葡萄糖相比,钾的存在刺激了cl的吸收。此外,氯化物比硝酸盐和葡萄糖酸盐更能促进钾(86Rb)的吸收。钾梯度和缬霉素都没有进一步刺激这些过程,这表明存在电中性的K-Cl共转运系统。镁诱导的氯离子电导也在基底外侧膜泡中被发现。在没有镁的情况下,氯离子电导较低;valinomycin和向内钾梯度不刺激36Cl的摄取,蒽-9-羧酸不抑制36Cl的摄取,valinomycin不刺激氯依赖性86Rb的摄取。然而,在1 mM镁的存在下,得到相反的结果;valinomycin和向内钾梯度刺激36Cl的摄取,蒽-9-羧酸抑制36Cl的摄取,valinomycin刺激氯依赖性86Rb的摄取。因此,在兔肾皮质制备的肾皮质基底外侧膜囊中发现了电中性的K-Cl共转运和镁诱导的氯离子电导。
The transport pathways for chloride in basolateral membrane vesicles from the rabbit renal cortex were investigated. 36Cl uptake was stimulated by the presence of potassium in the uptake media compared with sodium or N-methyl-D-glucamine. In addition, potassium (86Rb) uptake was stimulated more by chloride than by nitrate or gluconate. Neither of these processes was further stimulated by potassium gradients plus valinomycin, suggesting the presence of an electrically neutral K-Cl cotransport system. A magnesium-induced chloride conductance was also found in the basolateral membrane vesicles. In the absence of magnesium, the chloride conductance was low; valinomycin and an inwardly directed potassium gradient did not stimulate 36Cl uptake, anthracene-9-carboxylic acid did not inhibit 36Cl uptake, and valinomycin did not stimulate chloride-dependent 86Rb uptake. However, in the presence of 1 mM magnesium, opposite results were obtained; valinomycin and an inwardly directed potassium gradient stimulated 36Cl uptake, anthracene-9-carboxylic acid inhibited 36Cl uptake, and valinomycin stimulated chloride-dependent 86Rb uptake. Therefore, an electrically neutral K-Cl cotransport and magnesium-induced chloride conductance were found in renal cortical basolateral membrane vesicles prepared from the rabbit renal cortex.