代谢性酸中毒时分离的肾刷状缘膜囊泡中的钠氢交换。动力学效应。
Na+-H+ exchange in isolated renal brush-border membrane vesicles in response to metabolic acidosis. Kinetic effects.
作者信息
Kinsella J, Cujdik T, Sacktor B
出版信息
J Biol Chem. 1984 Nov 10;259(21):13224-7.
Chronic metabolic acidosis increased the Na+-H+ exchange activity in isolated renal brush-border membrane vesicles. Treatment altered the initial rate of Na+ uptake by increasing Vm (acidotic, 15.3 +/- 0.7 nmol of Na+ X mg-1 X 2 s-1; normal, 11.3 +/- 0.9 nmol of Na+ X mg-1 X 2 s-1), and not the apparent affinity KNa+ (acidotic, 10.2 +/- 0.5 mM; normal 10.2 +/- 0.6 mM). Metabolic acidosis resulted in the proportional increase in 1 mM Na+ uptake at every intravesicular pH measured. A positive cooperative effect on Na+ uptake was found with increased intravesicular acidity in vesicles from both normal and acidotic rats. When the data were analyzed by the Hill equation, it was found that metabolic acidosis did not change the n (acidotic, 1.33 +/- 0.13; normal, 1.43 +/- 0.07) or the K'H+ (acidotic, 0.27 +/- 0.05 microM; normal, 0.28 +/- 0.06 microM), but increased the apparent Vm (acidotic, 1.10 +/- 0.08 nmol of Na+ X mg-1 X 2 s-1; normal, 0.81 +/- 0.07 nmol of Na+ X mg-1 X 2 s-1). The uptake of Na+ in exchange for H+ in membrane vesicles from normal and acidotic animals was not influenced by membrane potential. We conclude that metabolic acidosis leads to either an increase in the number of functioning exchangers or an increase in the turnover rate of the limiting step in the exchange.
慢性代谢性酸中毒增加了离体肾刷状缘膜囊泡中的Na⁺-H⁺交换活性。处理通过增加Vm改变了Na⁺摄取的初始速率（酸中毒组，15.3±0.7 nmol Na⁺×mg⁻¹×2 s⁻¹；正常组，11.3±0.9 nmol Na⁺×mg⁻¹×2 s⁻¹），而不是表观亲和力KNa⁺（酸中毒组，10.2±0.5 mM；正常组，10.2±0.6 mM）。代谢性酸中毒导致在每个测量的囊泡内pH值下，1 mM Na⁺摄取量成比例增加。在正常和酸中毒大鼠的囊泡中，随着囊泡内酸度增加，发现对Na⁺摄取有正协同效应。当用希尔方程分析数据时，发现代谢性酸中毒并未改变n（酸中毒组，1.33±0.13；正常组，1.43±0.07）或K'H⁺（酸中毒组，0.27±0.05 μM；正常组，0.28±0.06 μM），但增加了表观Vm（酸中毒组，1.10±0.08 nmol Na⁺×mg⁻¹×2 s⁻¹；正常组，0.81±0.07 nmol Na⁺×mg⁻¹×2 s⁻¹）。正常和酸中毒动物的膜囊泡中Na⁺与H⁺交换的摄取不受膜电位影响。我们得出结论，代谢性酸中毒导致功能正常的交换体数量增加或交换中限速步骤的周转率增加。
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