首页> 美国卫生研究院文献>The Journal of Physiology >Sodium-hydrogen ion exchange in rabbit renal cortical slices incubated in acetate media.
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Sodium-hydrogen ion exchange in rabbit renal cortical slices incubated in acetate media.

机译:在醋酸盐培养基中孵育的兔肾皮质切片中的钠氢离子交换。

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摘要

1. Thin slices (0.2-0.3 mm) of rabbit renal cortex have been incubated in isosmotic oxygenated acetate media at 25 degrees C with or without ouabain (10(-3) M), amiloride (2 x 10(-3) M) or iodoacetamide (10(-3) M). 2. Slices in normal isosmotic 146 mM-sodium-132 mM-acetate media swelled as reported previously (Cooke & Macknight, 1984). This swelling was not prevented by amiloride or by metabolic inhibition. 3. Slices in isosmotic 132 mM-choline-132 mM-acetate media gained much less water and were little affected by ouabain, amiloride or metabolic inhibition. Choline was able to substitute neither for sodium nor for potassium in activating preparations of renal cortical Na+-K+-ATPase in chloride or in acetate media. 4. Slices in isosmotic 20 mM-sodium-132 mM-acetate medium swelled nearly as much as did slices in normal sodium acetate medium. However, this swelling was impaired markedly by amiloride, by ouabain and by metabolic inhibition. 5. There was a direct correlation between medium sodium concentration and slice water content as sodium was increased from 1.25 to 30 mM in 132 mM-acetate media. However, up to a sodium concentration of 10 mM, amiloride (2 x 10(-3) M) completely prevented this increase in water content. 6. Increasing medium amiloride concentration from 10(-5) to 10(-3) M progressively inhibited cellular swelling in 10 mM-sodium-132 mM-acetate medium. It is concluded that, under these experimental conditions, the dominant pathway for hydrogen ion extrusion from the cells was via amiloride-sensitive sodium-hydrogen exchange. 7. The results are discussed in terms of a model which explains cellular swelling in acetate media in terms of (a) non-ionic diffusion of acetic acid across plasma membranes impermeable to the acetate anion, (b) removal from the cells of the hydrogen ion gained with the acetate by amiloride-sensitive sodium-hydrogen counter-transport and (c) subsequent extrusion of sodium from the cell accompanied by potassium uptake via the ouabain-sensitive Na+-K+-ATPase. 8. The results provide evidence for ion movements across the luminal plasma membrane of proximal tubular cells in rabbit renal cortical slices.
机译:1.将兔子肾皮质的薄片(0.2-0.3毫米)在等渗含氧乙酸盐介质中于25°C下孵育,无论有无哇巴因(10(-3)M),阿米洛利(2 x 10(-3)M)或碘乙酰胺(10(-3)M)。 2.正常等渗的146 mM-132 mM-乙酸钠培养基中的切片如先前报道的那样溶胀(Cooke&Macknight,1984)。阿米洛利或新陈代谢的抑制作用并不能阻止这种肿胀。 3.在等渗的132 mM-胆碱-132 mM-乙酸盐培养基中的切片获得的水少得多,并且几乎不受哇巴因,阿米洛利或代谢抑制的影响。在氯化物或乙酸盐介质中激活肾皮质Na + -K + -ATPase制剂中,胆碱既不能替代钠也不能替代钾。 4.等渗的20 mM-132 mM-乙酸钠培养基中的切片溶胀几乎与普通乙酸钠培养基中的切片溶胀一样多。然而,阿米洛利,哇巴因和新陈代谢抑制显着削弱了这种肿胀。 5.随着钠在132 mM醋酸盐培养基中从1.25 mM增加到30 mM,中钠浓度与切片水分含量之间存在直接相关性。但是,最高钠浓度为10 mM时,阿米洛利(2 x 10(-3)M)完全阻止了水含量的这种增加。 6.在10 mM-132 mM乙酸钠培养基中,阿米洛利培养基的浓度从10(-5)增加到10(-3)M逐渐抑制细胞肿胀。结论是,在这些实验条件下,氢离子从细胞中挤出的主要途径是通过阿米洛利敏感的钠氢交换。 7.以模型的形式讨论了结果,该模型以下列方式解释了乙酸盐介质中的细胞溶胀:(a)乙酸跨乙酸酯阴离子不可渗透的质膜的非离子扩散,(b)从氢电池中去除通过阿米洛利敏感的钠-氢反向转运与乙酸盐获得的离子;(c)随后从细胞中挤出钠,并通过哇巴因敏感的Na + -K + -ATPase吸收钾。 8.结果提供了离子在兔肾皮质切片中的近端肾小管腔的质膜上运动的证据。

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