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美洲鳗螈红细胞的体积调节:胞质游离钙与碱金属 - 氢交换

Volume regulation by Amphiuma red blood cells: cytosolic free Ca and alkali metal-H exchange.

作者信息

Cala P M, Mandel L J, Murphy E

出版信息

Am J Physiol. 1986 Mar;250(3 Pt 1):C423-9. doi: 10.1152/ajpcell.1986.250.3.C423.

Abstract

Osmotic swelling of Amphiuma red blood cells results in activation of electroneutral K-H exchange, whereas cell shrinkage activates an electroneutral Na-H exchange. These K-H and Na-H exchangers function to restore cell volume to normal after cell swelling and shrinkage, respectively. Our previous studies have suggested that Ca plays a role in volume-dependent activation of K-H exchange. In the present studies, intracellular free Ca levels were measured employing the Ca-sensitive extracellular dye arsenazo III and a previously described null-point method. Control values for intracellular free Ca averaged 0.46 +/- 0.15 microM. Cell shrinkage caused this value to decrease to 0.16 +/- 0.11 microM, whereas either cell swelling or addition of 5 microM A23187 resulted in saturation of intracellular Ca buffers, suggesting that both treatments caused an increase in intracellular free Ca. In the presence of 7 microM A23187, the rate of K-H exchange displayed a hyperbolic relationship as a function of extracellular Ca (Cao). The apparent half-maximal concentration for Cao (in the presence of 7 microM A23187) was 0.27 mM for osmotically swollen cells and 1.9 mM for cells in isotonic medium, suggesting that the Ca affinity of a modulating site is increased in swollen cells. Inhibitors of Ca-mediated processes, such as quinidine and the phenothiazines, inhibited K-H exchange. In contrast, the phenothiazines chlorpromazine and trifluoperazine stimulated Na-H exchange by osmotically shrunken cells. These results suggest that increases in intracellular free Ca are involved in stimulating K-H exchange while repressing Na-H exchange in Amphiuma red blood cells.

摘要

美洲鳗螈红细胞的渗透性肿胀会导致电中性钾氢交换的激活,而细胞收缩则会激活电中性钠氢交换。这些钾氢和钠氢交换体的作用分别是在细胞肿胀和收缩后将细胞体积恢复到正常水平。我们之前的研究表明,钙在钾氢交换的体积依赖性激活中起作用。在本研究中,采用钙敏感的细胞外染料偶氮胂III和先前描述的零点法测量细胞内游离钙水平。细胞内游离钙的对照值平均为0.46±0.15微摩尔。细胞收缩导致该值降至0.16±0.11微摩尔,而细胞肿胀或添加5微摩尔A23187都会导致细胞内钙缓冲剂饱和,这表明两种处理都会导致细胞内游离钙增加。在存在7微摩尔A23187的情况下,钾氢交换速率与细胞外钙(Cao)呈双曲线关系。对于渗透性肿胀的细胞,Cao的表观半最大浓度(在存在7微摩尔A23187的情况下)为0.27毫摩尔,对于等渗培养基中的细胞为1.9毫摩尔,这表明肿胀细胞中调节位点的钙亲和力增加。钙介导过程的抑制剂,如奎尼丁和吩噻嗪类药物,会抑制钾氢交换。相反,吩噻嗪类药物氯丙嗪和三氟拉嗪会刺激渗透性收缩细胞的钠氢交换。这些结果表明,细胞内游离钙的增加参与刺激美洲鳗螈红细胞的钾氢交换,同时抑制钠氢交换。

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