Maddox D A, Fortin S M, Tartini A, Barnes W D, Gennari F J
Department of Medicine, University of Vermont College of Medicine, Burlington 05405.
J Clin Invest. 1992 Apr;89(4):1296-303. doi: 10.1172/JCI115715.
Studies were undertaken in Munich-Wistar rats to assess the influence of changes in filtered bicarbonate (FLHCO3), induced by changes in GFR, on Na+/H+ exchange activity in renal brush border membrane vesicles (BBMV). Whole-kidney and micropuncture measurements of GFR, FLHCO3, and whole-kidney and proximal tubule HCO3 reabsorption (APRHCO3) were coupled with BBMV measurements of H+ gradient-driven 22Na+ uptake in each animal studied. 22Na+ uptake was measured at three Na+ concentration gradients to allow calculation of Vmax and Km for Na+/H+ exchange. GFR was varied by studying animals under conditions of hydropenia, plasma repletion, and acute plasma expansion. The increase in GFR, FLHCO3, and APRHCO3 induced by plasma administration correlated directly with an increase in the Vmax for Na+/H+ exchange in BBMV. The Km for sodium was unaffected. In the plasma-expanded rats, the Vmax for Na+/H+ exchange was 22% greater than in the hydropenic rats (P less than 0.025) whereas APRHCO3 was 86% greater (P less than 0.001). These results indicate that increases in FLHCO3, induced by acute increases in GFR, stimulate Na+/H+ exchange activity in proximal tubular epithelium. This stimulation is a mechanism which can, in part, account for the delivery dependence of proximal bicarbonate reabsorption.
在慕尼黑-威斯塔大鼠身上进行了多项研究，以评估肾小球滤过率（GFR）变化引起的滤过碳酸氢盐（FLHCO3）变化对肾刷状缘膜囊泡（BBMV）中Na+/H+交换活性的影响。对每只研究动物进行了全肾和微穿刺测量GFR、FLHCO3，以及全肾和近端小管HCO3重吸收（APRHCO3），同时结合BBMV测量H+梯度驱动的22Na+摄取。在三个Na+浓度梯度下测量22Na+摄取，以便计算Na+/H+交换的Vmax和Km。通过在缺水、血浆补充和急性血浆扩容条件下研究动物来改变GFR。血浆输注引起的GFR、FLHCO3和APRHCO3增加与BBMV中Na+/H+交换的Vmax增加直接相关。钠的Km不受影响。在血浆扩容的大鼠中，Na+/H+交换的Vmax比缺水大鼠高22%（P<0.025），而APRHCO3高86%（P<0.001）。这些结果表明，GFR急性增加引起的FLHCO3增加刺激近端肾小管上皮细胞中的Na+/H+交换活性。这种刺激是一种机制，部分可以解释近端碳酸氢盐重吸收对输送的依赖性。
