Borgese F, Garcia-Romeu F, Motais R
J Gen Physiol. 1986 Apr;87(4):551-66. doi: 10.1085/jgp.87.4.551.
It has previously been shown (Baroin, A., F. Garcia-Romeu, T. Lamarre, and R. Motais. 1984a, b. Journal of Physiology. 350:137, 356:21; Mahé, Y., F. Garcia-Romeu, and R. Motais. 1985. European Journal of Pharmacology. 116:199) that the addition of catecholamines to an isotonic suspension of nucleated red blood cells of the rainbow trout first stimulates a cAMP-dependent, amiloride-sensitive Na+/H+ exchange. This stimulation seems to be transient. It is followed by a more permanent activation of a coupled entry of Na+ and Cl-, which is inhibited by amiloride but also by inhibitors of band 3 protein (DIDS, furosemide, niflumic acid). The coupled entry of Na+ and Cl- could therefore result from the parallel and simultaneous exchange of Na+out for H+in (via the cAMP-dependent Na+/H+ antiporter) and Cl- out for HCO3- in (via the anion exchange system located in band 3 protein). However, in view of the following arguments, it had been proposed that NaCl uptake does not proceed by the double-exchanger system but via an NaCl cotransport: (a) Na+ entry requires Cl- as anion (in NO3- medium, the Na uptake is strongly inhibited, whereas NO3- is an extremely effective substitute for Cl- in the anion exchange system); (b) Na uptake is not significantly affected by the presence of HCO3- in the suspension medium despite the fact that in red cells, Cl-/HCO3- exchange occurs more readily than the exchanges of Cl- for basic equivalents in a theoretically CO2-free medium (the so-called Cl-/OH- exchanges). The purpose of the present paper was a reassessment of the two models by using monensin, an ionophore allowing Na+/H+ exchange. From this study, it appears that NaCl entry results from the simultaneous functioning of the Na+/H+ antiporter and the anion exchange system. The apparent Cl dependence is explained by the fact that, in these erythrocytes, NO3- clearly inhibits the turnover rate of the Na+/H+ antiporter. As Na+/H+ exchange is the driving component in the salt uptake process, this inhibition explains the Cl requirement for Na entry. The lack of stimulation of cell swelling by bicarbonate is explained by the fact that the rate of anion exchange in a CO2-free medium (Cl-/OH- exchange) is roughly equivalent to that of Na+/H+ exchange and thus in practice is not limiting to the net influx of NaCl through the two exchangers.(ABSTRACT TRUNCATED AT 400 WORDS)
此前已有研究表明（巴罗因，A.，F. 加西亚 - 罗梅乌，T. 拉马尔，和 R. 莫泰斯。1984 年 a、b 卷。《生理学杂志》。350:137，356:21；马赫，Y.，F. 加西亚 - 罗梅乌，和 R. 莫泰斯。1985 年。《欧洲药理学杂志》。116:199），向虹鳟有核红细胞的等渗悬浮液中添加儿茶酚胺首先会刺激一种依赖 cAMP、对氨氯吡脒敏感的 Na⁺/H⁺交换。这种刺激似乎是短暂的。随后是 Na⁺和 Cl⁻耦合进入的更持久激活，氨氯吡脒以及带 3 蛋白抑制剂（二异丙基氨基磺酸钠、速尿、氟尼酸）均可抑制该过程。因此，Na⁺和 Cl⁻的耦合进入可能是由于 Na⁺外流与 H⁺内流（通过依赖 cAMP 的 Na⁺/H⁺反向转运体）以及 Cl⁻外流与 HCO₃⁻内流（通过位于带 3 蛋白中的阴离子交换系统）同时并行交换的结果。然而，鉴于以下论点，有人提出 NaCl 的摄取并非通过双交换系统进行，而是通过 NaCl 共转运：（a）Na⁺进入需要 Cl⁻作为阴离子（在 NO₃⁻介质中，Na⁺摄取受到强烈抑制，而在阴离子交换系统中 NO₃⁻是 Cl⁻的极其有效的替代物）；（b）尽管在红细胞中，在理论上无 CO₂的介质中 Cl⁻/HCO₃⁻交换比 Cl⁻与碱性等价物的交换（所谓的 Cl⁻/OH⁻交换）更容易发生，但悬浮介质中 HCO₃⁻的存在对 Na⁺摄取没有显著影响。本文的目的是通过使用莫能菌素（一种允许 Na⁺/H⁺交换的离子载体）对这两种模型进行重新评估。从这项研究来看，NaCl 的进入似乎是 Na⁺/H⁺反向转运体和阴离子交换系统同时作用的结果。明显的 Cl⁻依赖性可以解释为，在这些红细胞中，NO₃⁻明显抑制了 Na⁺/H⁺反向转运体的周转率。由于 Na⁺/H⁺交换是盐摄取过程中的驱动成分，这种抑制解释了 Na⁺进入对 Cl⁻的需求。碳酸氢盐对细胞肿胀缺乏刺激作用可以解释为，在无 CO₂的介质中阴离子交换速率（Cl⁻/OH⁻交换）大致等同于 Na⁺/H⁺交换速率，因此实际上并不限制 NaCl 通过这两种交换体的净内流。（摘要截断于 400 字）
