Cheeseman C I
J Physiol. 1983 May;338:87-97. doi: 10.1113/jphysiol.1983.sp014662.
The transport of the dibasic amino acid L-lysine across the serosal pole of the intestinal epithelium has been studied using the vascularly perfused anuran small intestine. The exit of pre-loaded lysine into the vascular bed was inhibited by L-ornithine (2 mM) and L-arginine (10 mM) when pulsed through the lumen during the wash-out, while 2-aminoisobutyric acid (AIB), L-histidine, L-citrulline and L-cystine had no effect. Luminal L-leucine and L-alanine at a concentration of 10 mM markedly stimulated the unloading of lysine into the vascular bed and sarcosine, L-proline and beta-alanine also did so to a lesser extent. The instantaneous rate constant for lysine exit into the vascular bed was increased by the presence of L-arginine, L-ornithine, L-citrulline, L-histidine, AIB, L-leucine and L-alanine at a concentration of 10 mM in the vascular bed. L-proline had no effect. The simultaneously measured efflux of lysine into the lumen was unaffected by the presence of the other amino acids in the vascular bed. The uptake of lysine into the epithelium from the vascular bed was accelerated by L-ornithine and slightly by L-arginine when they were present in the lumen, while L-leucine, L-alanine, beta-alanine, L-proline, L-citrulline, sarcosine, L-histidine and AIB had no effect. The instantaneous rate constant for lysine wash-out into the vascular bed was transiently increased by the presence of L-leucine in the vascular bed at concentrations of 10, 0.10 and 0.01 mM. The steady-state transfer of lysine from the lumen to the vascular bed was stimulated in a biphasic manner by 5 mM-leucine in the lumen and by 0.5 mM-leucine in the vascular bed. The mechanisms for these interactions between lysine transport across the basolateral membrane of the enterocyte and other amino acids are discussed and a possible role for neutral amino acid stimulation of lysine exit is proposed.
利用血管灌注的无尾两栖类小肠，对二氨基氨基酸L-赖氨酸跨肠上皮细胞浆膜极的转运进行了研究。在洗脱过程中，当通过肠腔脉冲注入L-鸟氨酸（2 mM）和L-精氨酸（10 mM）时，预先装载的赖氨酸向血管床的排出受到抑制，而2-氨基异丁酸（AIB）、L-组氨酸、L-瓜氨酸和L-胱氨酸则没有影响。浓度为10 mM的肠腔L-亮氨酸和L-丙氨酸显著刺激了赖氨酸向血管床的卸载，肌氨酸、L-脯氨酸和β-丙氨酸在较小程度上也有此作用。血管床中浓度为10 mM的L-精氨酸、L-鸟氨酸、L-瓜氨酸、L-组氨酸、AIB、L-亮氨酸和L-丙氨酸的存在增加了赖氨酸进入血管床的瞬时速率常数。L-脯氨酸没有影响。同时测得的赖氨酸向肠腔的流出不受血管床中其他氨基酸存在的影响。当L-鸟氨酸存在于肠腔中时，它会加速赖氨酸从血管床进入上皮细胞的摄取，L-精氨酸也有轻微作用，而L-亮氨酸、L-丙氨酸、β-丙氨酸、L-脯氨酸、L-瓜氨酸、肌氨酸、L-组氨酸和AIB则没有影响。血管床中浓度为10、0.10和0.01 mM的L-亮氨酸的存在会使赖氨酸向血管床洗脱的瞬时速率常数短暂增加。肠腔中5 mM的亮氨酸和血管床中0.5 mM的亮氨酸以双相方式刺激了赖氨酸从肠腔到血管床的稳态转运。讨论了赖氨酸跨肠上皮细胞基底外侧膜转运与其他氨基酸之间这些相互作用的机制，并提出了中性氨基酸刺激赖氨酸排出的可能作用。
