Watkins C A, Mylin L M, Rannels D E
Biochem J. 1986 Apr 1;235(1):33-8. doi: 10.1042/bj2350033.
Na+-dependent uptake of 5-HT (5-hydroxytryptamine) into plasma membrane vesicles derived from bovine blood platelets and ATP-dependent 5-HT uptake into storage vesicles in platelet lysates were measured. Na+-dependent uptake was temperature-dependent, inhibited by imipramine and exhibited Michaelis-Menten kinetics (apparent Km, 0.12 +/- 0.02 microM; Vmax. 559 +/- 54 pmol/min per mg of protein. Halothane had no effect on Na+-dependent transport of 5-HT in plasma-membrane vesicles. ATP-dependent 5-HT transport into storage granules also exhibited Michaelis-Menten kinetics (apparent Km 0.34 +/- 0.03 microM; Vmax. 34.3 +/- 1.7 pmol/min per mg of protein) and was inhibited by noradrenaline (norepinephrine), but not by imipramine. Exposure of the granules to halothane resulted in a progressive decrease in Vmax. The results demonstrate a possible site for disruption of platelet function by anaesthetics.
测定了牛血小板来源的质膜囊泡中5-羟色胺（5-HT）的钠依赖性摄取以及血小板裂解物中5-HT进入储存囊泡的ATP依赖性摄取。钠依赖性摄取是温度依赖性的，受丙咪嗪抑制，并表现出米氏动力学（表观Km，0.12±0.02微摩尔；Vmax，559±54皮摩尔/分钟/毫克蛋白质）。氟烷对质膜囊泡中5-HT的钠依赖性转运没有影响。5-HT进入储存颗粒的ATP依赖性转运也表现出米氏动力学（表观Km 0.34±0.03微摩尔；Vmax，34.3±1.7皮摩尔/分钟/毫克蛋白质），并受去甲肾上腺素抑制，但不受丙咪嗪抑制。将颗粒暴露于氟烷导致Vmax逐渐降低。结果表明麻醉剂可能破坏血小板功能的位点。
