Martin M, Ferrier B, Baverel G
Institut National de la Santé et de la Recherche Médicale (U 80), Lyon, France.
Pflugers Arch. 1989 Jan;413(3):217-24. doi: 10.1007/BF00583533.
In order to establish the characteristics of net renal transport and utilization of alpha-ketoglutarate (alpha-KG) in the rat, we have precisely quantified the renal blood flow, the urinary flow and the rates of alpha-KG delivery, filtration, reabsorption or secretion, excretion, uptake or production by an in vivo rat kidney preparation. In normal rats, alpha-KG uptake was higher than alpha-KG reabsorption at both endogenous and elevated plasma alpha-KG concentrations; thus, a net peritubular transport, which was the main supplier of alpha-KG to the renal cells, took place. Saturation of reabsorption and peritubular transport of alpha-KG occurred at blood alpha-KG concentrations about 30 and 150 times above normal, respectively. Acute metabolic acidosis was found to have no effect on renal handling of alpha-KG. At endogenous plasma alpha-KG concentrations, alkalosis converted net renal uptake into net renal production of alpha-KG resulting in addition of alpha-KG by the renal cells both to blood and to the luminal fluid. Elevation of blood alpha-KG concentration restored the renal uptake of alpha-KG. This uptake, which was entirely accounted for by the peritubular transport of alpha-KG, reached a maximum which was lower than that observed in normal and acidotic rats.
为了确定大鼠肾脏对α-酮戊二酸(α-KG)的净转运和利用特性,我们通过大鼠肾脏活体标本精确测定了肾血流量、尿流量以及α-KG的输送、滤过、重吸收或分泌、排泄、摄取或生成速率。在正常大鼠中,无论是内源性还是血浆α-KG浓度升高时,α-KG的摄取均高于α-KG的重吸收;因此,发生了肾小管周围的净转运,这是α-KG向肾细胞的主要供应途径。α-KG重吸收和肾小管周围转运的饱和分别发生在血液α-KG浓度比正常水平高约30倍和150倍时。发现急性代谢性酸中毒对肾脏处理α-KG没有影响。在内源性血浆α-KG浓度下,碱中毒将肾脏的净摄取转化为α-KG的净生成,导致肾细胞将α-KG添加到血液和管腔液中。血液α-KG浓度升高可恢复肾脏对α-KG的摄取。这种摄取完全由α-KG的肾小管周围转运引起,达到的最大值低于正常和酸中毒大鼠中观察到的最大值。