Cardelli-Cangiano P, Cangiano C, James J H, Ceci F, Fischer J E, Strom R
J Biol Chem. 1984 Apr 25;259(8):5295-300.
NH+4 ions, at a concentration (0.25 mM) similar to that found in the plasma of patients with hepatic encephalopathy, cause, in vitro, a significant stimulation of the uptake by brain microvessels of large neutral amino acids, without any effect on the uptake of alpha-methylaminoisobutyric acid, glutamic acid, or lysine. Such a stimulation occurs essentially through an increase of the maximal transport capacity (Vmax) of the saturable component. It is apparently mediated by the intracellular formation of glutamine, which is then exchanged, through the L-system of transport, for large neutral amino acids such as leucine, phenylalanine, or tyrosine. At higher concentrations (greater than or equal to 0.5 mM), NH+4 ions cause also a decrease of carrier affinity for neutral amino acids, which counteracts the stimulatory effect on their uptake.
铵离子浓度（0.25 mM）与肝性脑病患者血浆中的浓度相似，在体外可显著刺激脑微血管对大中性氨基酸的摄取，而对α-甲基氨基异丁酸、谷氨酸或赖氨酸的摄取没有任何影响。这种刺激主要通过可饱和成分的最大转运能力（Vmax）增加而发生。这显然是由谷氨酰胺的细胞内形成介导的，然后谷氨酰胺通过L转运系统与亮氨酸、苯丙氨酸或酪氨酸等大中性氨基酸进行交换。在较高浓度（大于或等于0.5 mM）时，铵离子也会导致载体对中性氨基酸的亲和力降低，这抵消了对其摄取的刺激作用。
