Allis J L, Endre Z H, Radda G K
Department of Biochemistry, University of Oxford, UK.
Ren Physiol Biochem. 1989 May-Jun;12(3):171-80.
87Rb, 23Na and 31P nuclear magnetic resonance (NMR) were used to monitor changes in renal cations and energetics during the induction of hypoxia in the isolated perfused rat kidney. The NMR-determined unidirectional Rb+ flux in normoxic kidneys was shown to be a good measure of net intracellular K+ influx in the perfused rat kidney model. The changes in 87Rb, 23Na and 31P spectra following the induction of hypoxia are consistent with hypoxic depletion of intracellular adenosine triphosphate (ATP) and a subsequent decrease in Na-K-ATPase transport activity. The exponential rate constant for 87Rb+ efflux measured during Rb+ uptake in normoxic kidneys (0.12 +/- 0.01 min-1) was not significantly different to the rate constant for 87Rb+ efflux during the induction of hypoxia (0.16 +/- 0.07 min-1). We conclude that there is no direct effect of hypoxia on renal cellular membrane integrity and that renal cell sensitivity to hypoxia is due to an inability to sustain cellular ion gradients following depletion of intracellular ATP.
利用87Rb、23Na和31P核磁共振（NMR）技术监测离体灌流大鼠肾脏在诱导缺氧过程中肾阳离子和能量代谢的变化。在常氧肾脏中，NMR测定的单向Rb+通量被证明是灌流大鼠肾脏模型中细胞内净K+流入的良好指标。缺氧诱导后87Rb、23Na和31P光谱的变化与细胞内三磷酸腺苷（ATP）的缺氧消耗以及随后钠钾ATP酶转运活性的降低相一致。在常氧肾脏中Rb+摄取期间测得的87Rb+流出的指数速率常数（0.12±0.01 min-1）与缺氧诱导期间87Rb+流出的速率常数（0.16±0.07 min-1）无显著差异。我们得出结论，缺氧对肾细胞膜完整性没有直接影响，肾细胞对缺氧的敏感性是由于细胞内ATP耗尽后无法维持细胞离子梯度所致。
