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目的比较自发性高血压大鼠（SHR）、肾动脉狭窄型高血压大鼠（2K1C）及相应的对照大鼠（WKY）静注苯丙氨酸的药代动力学。方法测定静注［~3H］标记的苯丙氨酸后不同时间大鼠血液及不同组织中放射性计数，进行药代动力学拟合及计算。结果大鼠中苯丙氨酸的药物动力学符合两室开放模型。SHR中苯丙氨酸清除半衰期为96±17min，清除率为56±14ml／kg·min~-1，药时曲线下面积为311±79ng／ml·min~-1，表观分布容积为490±80ml／kg，心脏和主动脉壁中苯丙氨酸含量分别为1．7±0.4及4．9±1.7pg／mg，与WKY相比差异显著（P＜0.05）。2K1C与WKY相比除肝脏中苯丙氨酸含量增加外均无显著差别。结论苯丙氨酸在SHR中的消除较WKY中减慢，其原因可能是遗传所致，而不是血压升高所引起。
Objective To compare the pharmacokinetics of phenylalanine in spontaneously hypertensive rats (SHR), renal artery stenosis hypertensive rats (2K1C) and corresponding control rats (WKY). Methods Radioimmunoassay was performed in rat blood and different tissues at different time points after [~ 3H] - labeled phenylalanine injection. The pharmacokinetics were fitted and calculated. Results The pharmacokinetics of phenylalanine in rats was in accordance with the two-compartment open model. The half-life of phenylalanine in SHR was 96 ± 17min, the clearance rate was 56 ± 14ml / kg · min ~ (-1), the area under the curve was 311 ± 79ng / ml · min ~ -1 and the apparent volume of distribution was 490 ± 80ml / kg. The contents of phenylalanine in heart and aortic wall were 1.7 ± 0.4 and 4.9 ± 1.7pg / mg, respectively, which were significantly different from those of WKY (P <0.05). There was no significant difference between 2K1C and WKY except for the increase of phenylalanine in the liver. Conclusion The elimination of phenylalanine in SHR is slower than that in WKY, which may be caused by genetics rather than by the increase of blood pressure.