Busch S, Burckhardt B C, Siffert W
Max-Planck-Institut für Biophysik, Frankfurt, Germany.
Pflugers Arch. 1995 Apr;429(6):859-69. doi: 10.1007/BF00374811.
We investigated whether the human sodium/proton (Na+/H+) exchanger isoform 1 (NHE-1) can mediate sodium/lithium (Na+/Li+) countertransport. Using the Xenopus laevis oocyte expression system we determined amiloride-sensitive Li+ uptake, a measure of Na+/H+ exchange, in oocytes injected with water or NHE-1 cRNA. Amiloride-sensitive Li+ uptake was three- to tenfold enhanced over control in NHE-1 cRNA-injected cells and was selectively inhibited by 0.01 microM HOE 694 [i.e. (3-methylsulphonyl-4-piperidinobenzoyl) guanidine methanesulphonate]. The endogenously present Na+/H+ exchanger was insensitive to HOE 694. After acidification of oocytes from pH 7.7 to 6.8, amiloride-sensitive Li+ uptake was four- to tenfold higher in NHE-1 cRNA-injected cells than in controls. Li+ efflux from control oocytes was independent of extracellular Na+, indicating that these cells expressed no measurable Na+/Li+ countertransport activity. In NHE-1 cRNA-injected oocytes, Li+ efflux was distinctly enhanced by extracellular Na+ ions. This Na(+)-dependent Li+ efflux was inhibited by ethylisopropylamiloride, phloretin and by cytosolic acidification. The data show that expression of the NHE-1 in X. laevis oocytes induces the expression of Na+/Li+ countertransport. The data confirm that Na+/H+ exchange and Na+/Li+ countertransport are mediated by the same transport system.
我们研究了人类钠/质子（Na+/H+）交换体同工型1（NHE-1）是否能介导钠/锂（Na+/Li+）逆向转运。利用非洲爪蟾卵母细胞表达系统，我们测定了注射水或NHE-1编码RNA（cRNA）的卵母细胞中对氨氯地平敏感的Li+摄取，这是一种Na+/H+交换的测量指标。在注射NHE-1 cRNA的细胞中，对氨氯地平敏感的Li+摄取比对照增强了三到十倍，并且被0.01微摩尔的HOE 694 [即(3-甲基磺酰基-4-哌啶基苯甲酰基)胍甲磺酸盐]选择性抑制。内源性存在的Na+/H+交换体对HOE 694不敏感。将卵母细胞从pH 7.7酸化至6.8后，注射NHE-1 cRNA的细胞中对氨氯地平敏感的Li+摄取比对照高四到十倍。对照卵母细胞的Li+外流与细胞外Na+无关，表明这些细胞没有可测量的Na+/Li+逆向转运活性。在注射NHE-1 cRNA的卵母细胞中，细胞外Na+离子明显增强了Li+外流。这种Na+依赖的Li+外流被乙基异丙基氨氯地平、根皮素和胞质酸化所抑制。数据表明，NHE-1在非洲爪蟾卵母细胞中的表达诱导了Na+/Li+逆向转运的表达。数据证实，Na+/H+交换和Na+/Li+逆向转运由同一转运系统介导。
