Effect of osmolarity on cation fluxes in medullary thick ascending limb cells.

Effect of osmolarity on cation fluxes in medullary thick ascending limb cells.
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DOI:
10.1152/ajprenal.1986.250.1.f176
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发表时间:
1986
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
J. Eveloff;J. Calamia
J. Eveloff;J. Calamia
中科院分区:
其他
文献类型:
--
作者:
J. Eveloff;J. Calamia

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高渗细胞外介质对呋塞米敏感的钠和钾流量的影响进行了研究,在离体细胞从兔髓厚的汉勒氏襻(mTALH)的升支。在对照孵育培养基中,呋塞米敏感的22 Na摄取为379.1 +/- 24.4 pmol。mg蛋白-1。min-1,呋塞米敏感的86 Rb摄取为30.5 +/- 16.9。速尿敏感的22 Na流量不受直接进入细胞的K梯度的刺激,相反,速尿敏感的86 Rb流量不受直接进入细胞的Na梯度的刺激。这些发现与Na-Cl共转运系统一致。在200 mM甘露醇存在下,呋塞米敏感的22 Na和86 Rb通量显著增加至919.4 +/- 76.6和106.1 +/- 29.2 pmol。mg蛋白-1。min-1。当培养介质的渗透压增加时,不仅呋塞米敏感通量增加,而且这些通量变得相互依赖,即,除去Na或K防止了另一种阳离子的呋塞米敏感通量的增加。这一发现与mTALH细胞中的Na-K-2Cl共转运系统一致。这些数据表明,钠-氯和钠-K-2Cl共转运系统可能是不同的功能相同的呋塞米敏感的共转运系统,它们的表达可能受到细胞体积的变化。
The effects of a hypertonic extracellular medium on furosemide-sensitive Na and K fluxes were studied in isolated cells from the rabbit medullary thick ascending limb of Henle's loop (mTALH). In the control incubation medium, the furosemide-sensitive 22Na uptake was 379.1 +/- 24.4 pmol . mg protein-1 . min-1 and the furosemide-sensitive 86Rb uptake was 30.5 +/- 16.9. The furosemide-sensitive 22Na flux was not stimulated by K gradients directed into the cells, and, conversely, the furosemide-sensitive 86Rb flux was not stimulated by Na gradients directed into the cells. These findings are consistent with a Na-Cl cotransport system. In the presence of 200 mM mannitol, the furosemide-sensitive 22Na and 86Rb fluxes were increased dramatically to 919.4 +/- 76.6 and 106.1 +/- 29.2 pmol . mg protein-1 . min-1, respectively. When the osmolarity of the incubation medium was increased, not only were the furosemide-sensitive fluxes increased but these fluxes became inter-dependent, i.e., removing Na or K prevented the increase in the furosemide-sensitive flux of the other cation. This finding is consistent with a Na-K-2Cl cotransport system in the mTALH cells. The data suggest that the Na-Cl and the Na-K-2Cl cotransport systems may be distinct functions of the same furosemide-sensitive cotransport system and that their expression may be regulated by changes in cell volume.