Characteristics of alpha-aminoisobutyric acid transport in rat skeletal muscles.
Characteristics of alpha-aminoisobutyric acid transport in rat skeletal muscles.
复制标题
大鼠骨骼肌中α-氨基异丁酸转运的特征。
DOI：
10.1042/bj2210071
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
D. Goldspink
中科院分区：
文献类型：
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作者：
S. E. Lewis;D. Goldspink
α-氨基异丁酸（AIB）转运到趾长伸肌和比目鱼肌的细胞内区室中，在允许氨基酸在细胞外空间中平衡后进行测量（体外）。后者用[~（14）C]菊粉、~（60）Co-EDTA和[~ 3 H]甘露醇三种标记物测定。AIB的净转运分为流入和流出两部分。内流率测量为短温育（5分钟）后[14 C]AIB的细胞内积累，外排率测量为AIB随时间（最多50分钟）从先前已预载AIB的肌肉中释放。这种细胞内流出分为两个阶段，这可能代表两个独立的组件退出。研究了细胞外Na+对这种中性氨基酸（代表A系统）转运的影响。Na+耗竭导致AIB的积累较低，随着外部Na+的逐渐耗竭，这种影响变得更加明显。这些变化是由于抑制AIB流入，同时增强其流出。相反，酪氨酸转运的所有组件（代表L系统）不受外部Na+浓度降低的影响。皮质醇也抑制AIB的净积累。然而，这种抑制作用是Na+依赖性的，并且仅仅是由于类固醇对AIB流出的增强，激素对AIB流入没有影响。
alpha-Aminoisobutyric acid (AIB) transport into the intracellular compartment of extensor digitorum longus and soleus muscles was measured (in vitro) after allowance for the equilibration of the amino acid in the extracellular space. The latter was determined with three markers, [14C]inulin, 60Co-EDTA and [3H]mannitol. Net transport of AIB was subsequently divided into its two components, i.e. influx and efflux. Rates of influx were measured as the intracellular accumulation of [14C]AIB after a short incubation (5 min), and efflux was measured as the release of AIB with time (up to maximum of 50 min) from muscles that had previously been preloaded with AIB. This intracellular efflux was resolved into two phases, which probably represent two separate components of exit. The influence of extracellular Na+ on the transport of this neutral amino acid (representing the A system) was investigated. Na+ depletion resulted in lower accumulations of AIB, the effects becoming more pronounced with progressive depletions of external Na+. These changes arose from an inhibition of AIB influx, concomitant with an enhancement of its efflux. In contrast, all components of tyrosine transport (representing the L system) were unaffected by lowering external Na+ concentrations. The net accumulation of AIB was also suppressed by cortisol. This inhibitory effect was, however, Na+-dependent and resulted solely from the steroid's enhancement of AIB efflux, the hormone being without effect on AIB influx.