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首页> 外文期刊>Kidney international. >L-Arginine transport is augmented through up-regulation of tubular CAT-2 mRNA in ischemic acute renal failure in rats
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L-Arginine transport is augmented through up-regulation of tubular CAT-2 mRNA in ischemic acute renal failure in rats

机译:L-精氨酸转运通过大鼠缺血性急性肾衰竭中肾小管CAT-2 mRNA的上调而增强

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L-Arginine transport is augmented through up-regulation of tubular CAT-2 mRNA in ischemic acute renal failure in rats.BackgroundIschemic acute renal failure (iARF) is associated with increased nitric oxide (NO) production during the reperfusion period, as endothelial nitric oxide synthase (eNOS) is maximally activated, and renal tubular inducible NOS (iNOS) is stimulated. Increased NO production leads to augmented tubular injury, probably through the formation of peroxynitrite. L-Arginine (L-Arg), the only precursor for NO, is transported into cells by cationic amino acid transporters, CAT-1 and CAT-2. We hypothesized that the increased NO production observed in iARF may result from increased L-Arg uptake, which would be reflected in the augmented expression of L-Arg transporter(s).
机译:缺血性急性肾衰竭大鼠肾小管中CAT-2 mRNA的上调增强了L-精氨酸的转运。合成酶(eNOS)被最大程度地激活,并且肾小管诱导型NOS(iNOS)被刺激。 NO产生增加可能导致过氧化亚硝酸盐形成,从而增加了肾小管损伤。 L-精氨酸(L-Arg)是NO的唯一前体,通过阳离子氨基酸转运蛋白CAT-1和CAT-2转运到细胞中。我们假设iARF中观察到的NO产生增加可能是由于L-Arg摄取增加所致,这将反映在L-Arg转运蛋白表达的增加上。

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