Kracke G R, Anatra M A, Dunham P B
Department of Biology, Syracuse University, New York 13244.
Am J Physiol. 1988 Feb;254(2 Pt 1):C243-50. doi: 10.1152/ajpcell.1988.254.2.C243.
The Na-K-Cl cotransport system in human erythrocytes was studied by measuring net influxes and effluxes of Na and K. The influx of K was shown to be stimulated by Na and the influx of Na was stimulated by K, satisfying the fundamental criterion of cotransport. In addition, these mutually stimulating cation influxes had a stoichiometry of 1:1 and were entirely inhibited by furosemide; these results are also consistent with cotransport. Furthermore, the mutually stimulating influxes were entirely dependent on Cl, since they were abolished when nitrate was substituted for Cl. In contrast, cotransport, defined by mutual dependence of fluxes, was not detected in the outward direction over a range of cellular Na and K concentrations from 0 to 50 mmol/l cells. The cotransport pathway did, however, appear to mediate a Na-stimulated K efflux (but no K-stimulated Na efflux), and furosemide-inhibitable effluxes of both Na and K. Nitrate (but not sulfate) appeared to substitute for chloride in promoting Na-stimulated K efflux. Thus the Na-K-Cl cotransport system in human red cells is intrinsically asymmetric, and mediates coupled cation fluxes readily only in the inward direction.
通过测量钠和钾的净内流和外流，对人类红细胞中的钠 - 钾 - 氯协同转运系统进行了研究。结果表明，钾的内流受钠刺激，钠的内流受钾刺激，符合协同转运的基本标准。此外，这些相互刺激的阳离子内流化学计量比为1:1，且完全被呋塞米抑制；这些结果也与协同转运一致。此外，相互刺激的内流完全依赖于氯，因为当用硝酸盐替代氯时，它们就会消失。相比之下，在细胞内钠和钾浓度从0到50 mmol/L的范围内，未检测到由通量相互依赖性定义的外向协同转运。然而，协同转运途径似乎介导了钠刺激的钾外流（但没有钾刺激的钠外流），以及呋塞米可抑制的钠和钾外流。硝酸盐（而非硫酸盐）似乎在促进钠刺激的钾外流方面可替代氯。因此，人类红细胞中的钠 - 钾 - 氯协同转运系统本质上是不对称的，并且仅在向内方向上容易介导耦合阳离子通量。
