Moe O W, Tejedor A, Levi M, Seldin D W, Preisig P A, Alpern R J
Department of Internal Medicine, University of Texas Southwestern, Medical Center, Dallas.
Am J Physiol. 1991 Jan;260(1 Pt 2):F130-7. doi: 10.1152/ajprenal.1991.260.1.F130.
An apical membrane Na(+)-H+ antiporter mediates proximal tubule NaCl and NaHCO3 reabsorption. The present studies examined whether chronic changes in dietary NaCl intake lead to an adaptation of the Na(+)-H+ antiporter. Rats were maintained either on a low-salt (LS, 0% NaCl) or a high-salt (HS, 2% NaCl) diet for 4 days. Na(+)-H+ antiporter was assayed using the acridine orange fluorescence method in apical membrane vesicles prepared by Mg2+ aggregation. Rats on LS diet exhibited a higher maximal activity (Vmax) for antiporter activity (0.109 +/- 0.008 s-1) compared with rats on HS diet (0.090 +/- 0.008 s-1; P less than 0.01), whereas Na activity (KNa) was similar (13.1 +/- 1.5 and 14.2 +/- 0.8 mM in HS and LS groups, respectively). The modulation of Na(+)-H+ antiporter activity was amiloride sensitive. Proton permeability, Na(+)-dependent [3H]glucose uptake, and vesicle enrichments were similar in both groups. In addition, the dietary protocols were not associated with any systemic acid-base disturbances, K+ deficiency, or hyperfiltration, conditions that have previously been demonstrated to alter Na(+)-H+ antiporter activity. Acute differences in extracellular fluid volume, induced by 10% body weight isohydric expansion failed to affect Na(+)-H+ antiporter activity. Thus chronic alterations in dietary NaCl intake alter the maximal activity (Vmax) of the Na(+)-H+ antiporter. This adaptation may contribute to decreased NaCl reabsorption in extracellular fluid volume expansion, enhanced NaCl reabsorption in extracellular fluid volume depletion, and enhanced NaHCO3 reabsorption in chronic metabolic alkalosis associated with volume contraction.
顶端膜钠氢交换体介导近端小管氯化钠和碳酸氢钠的重吸收。本研究检测了饮食中氯化钠摄入量的长期变化是否会导致钠氢交换体的适应性改变。将大鼠分别置于低盐（LS，0%氯化钠）或高盐（HS，2%氯化钠）饮食中饲养4天。使用吖啶橙荧光法在通过镁离子聚集制备的顶端膜囊泡中检测钠氢交换体。与HS饮食组大鼠（0.090±0.008 s-1；P<0.01）相比，LS饮食组大鼠的交换体活性最大活性（Vmax）更高（0.109±0.008 s-1），而钠活性（KNa）相似（HS组和LS组分别为13.1±1.5 mM和14.2±0.8 mM）。钠氢交换体活性的调节对氨氯地平敏感。两组的质子通透性、钠依赖性[3H]葡萄糖摄取和囊泡富集情况相似。此外，饮食方案与任何系统性酸碱紊乱、钾缺乏或超滤均无关，而这些情况此前已被证明会改变钠氢交换体活性。由10%体重等渗扩容引起的细胞外液体积急性差异未能影响钠氢交换体活性。因此，饮食中氯化钠摄入量的长期改变会改变钠氢交换体的最大活性（Vmax）。这种适应性变化可能有助于在细胞外液容量扩张时减少氯化钠重吸收，在细胞外液容量减少时增强氯化钠重吸收，以及在与容量收缩相关的慢性代谢性碱中毒时增强碳酸氢钠重吸收。
