首页> 外文期刊>Biochimica et biophysica acta. Biomembranes >Effect of ischemia reperfusion on sodium-dependent phosphate transport in renal brush border membranes
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Effect of ischemia reperfusion on sodium-dependent phosphate transport in renal brush border membranes

机译:缺血再灌注对肾刷缘膜钠依赖性磷酸盐转运的影响

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The effect of ischemia induced acute renal failure (ARF) on the transport of phosphate (Pi) after early (15-30 min) and prolonged (60 min) ischemia in the brush border membrane vesicles (BBMV) from rat renal cortex was studied. Sodium-dependent transport of Pi declined significantly and progressively due to ischemia. Western blot analysis of BBM from ischemic rats showed decreased expression of NaPi-2. A compensatory increase was observed in Pi uptake in BBMV from contralateral kidneys. There was no significant difference in NaPi-2 expression between BBMV from sham and contralateral kidneys. Early blood reperfusion for 15 min after 30 min ischemia caused further decline in Pi uptake. Prolonged reperfusion for 120 min caused partial reversal of transport activities in 30-min ischemic rats. However, no improvement in the transport of Pi was observed in 60-min ischemic rats after 120 min of blood reperfusion. Kinetic studies showed that the effect of ischemia and blood reperfasion was dependent on the V-max of the Na-Pi transporter. Western blot analysis showed increased expression of NaPi-2 in the BBMs from. ischemia-reperfusion animals. Further, a shift in the association of Na ions to transport one molecule of Pi was observed under different extracellular Na concentrations [Na](o). Feeding rats with low Pi diet and/or treatment with thyroid hormone (T3) prior to ischemia resulted in increased basal Pi transport. Ischemia caused similar decline in Pi transport in BBM from LPD and/or T3 animals. However, recovery in these animals was faster than the normal Pi diet fed (NPD) animals. The study suggests a change in the intrinsic properties of the Na-Pi transporter in rat kidneys due to ischemia. The study also indicates that treatment with T3 and feeding LPD prior to ischemia caused faster recovery of phosphate uptake due to ischemia-reperfusion injury. Published by Elsevier B.V.
机译:研究了缺血引起的急性肾衰竭(ARF)对大鼠肾皮质刷状缘膜囊泡(BBMV)早期(15-30分钟)和长时间(60分钟)缺血后磷酸盐(Pi)转运的影响。由于局部缺血,Pi的钠依赖性转运显着并逐渐下降。缺血大鼠BBM的Western印迹分析显示NaPi-2表达降低。观察到对侧肾脏的BBMV中Pi的摄取有补偿性增加。假和对侧肾脏的BBMV之间的NaPi-2表达没有显着差异。缺血30分钟后15分钟的早期血液再灌注导致Pi吸收进一步下降。长时间再灌注120分钟会导致30分钟缺血大鼠的运输活性部分逆转。然而,在血液再灌注120分钟后的60分钟缺血大鼠中,没有观察到Pi转运的改善。动力学研究表明,局部缺血和血液再灌注的影响取决于Na-Pi转运蛋白的V-max。蛋白质印迹分析显示NaPi-2在BBMs中表达增加。缺血再灌注动物。此外,在不同的细胞外Na浓度[Na](o)下,观察到Na离子缔合转运一个Pi分子的迁移。在缺血前用低Pi饮食喂养大鼠和/或用甲状腺激素(T3)治疗可导致基础Pi转运增加。缺血导致了来自LPD和/或T3动物的BBM中Pi转运的类似下降。但是,这些动物的恢复速度比正常的Pi饲喂(NPD)动物要快。研究表明,由于缺血,大鼠肾脏中Na-Pi转运蛋白的内在特性发生了变化。该研究还表明,由于缺血再灌注损伤,在缺血前用T3进行治疗并饲喂LPD可使磷酸盐吸收的恢复更快。由Elsevier B.V.发布

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