目的　研究CPU 86 0 17及L 甲状腺素对血管平滑肌收缩的影响及对α1A、α1B亚型的选择性。方法　以有钙、无钙液中由累积浓度去甲肾上腺素 (norepinephrine ,NE)引起的大鼠胸主动脉环的收缩 ,比较CPU 86 0 17(30 μmol·L-1)对正常及慢性甲状腺给药组 (Thy)大鼠血管平滑肌 (VSM)的α1受体的抑制作用。结果　在无钙液中由α1B引起的内钙释放所致VSM收缩占有钙液中VSM最大收缩的百分率 ,正常组和Thy组分别为 4 8 8%± 8 1%和 6 9.4 %± 9 7% (P <0 .0 1) ,复钙后由α1A引起的外钙内流所致VSM收缩百分率 ,分别为正常组 4 7 7%± 5 0 % ,Thy组为 2 2 1%± 9 4 % (P <0 .0 1)。加入CPU 86 0 17(30 μmol·L-1)后 ,对内钙释放所致的收缩 % ,正常对照组为 35 2 %± 10 1% ,Thy组为 35 2 %± 10 2 % ;而对外钙内流引起的收缩百分率则分别为 13 9%± 7 1%及 2 0 7%± 7 5 %。结论　L 甲状腺素使α1B的作用增强 ,而减弱α1A的作用。CPU 86 0 17在正常情况下对VSM的α1A的抑制强于α1B受体亚型 Objective To investigate the effect of CPU 86 0 17 and L thyroxine on the contraction of vascular smooth muscle and the selectivity of α1A and α1B subtypes. Methods The contractions of thoracic aortic rings caused by cumulative concentration of norepinephrine (NE) in calcium and calcium-free fluids were compared. The effects of CPU 86 0 17 (30 μmol·L-1) on normal and chronic thyroid Inhibitory effect of α1 receptor on vascular smooth muscle (VSM) of rats in the administration group. Results VSMC contraction caused by intracellular calcium release caused by α1B in calcium-free solution accounted for the largest percentage of VSM contraction in calcium solution, which was 488% ± 8 1% and 6 9.4% ± 9 7% respectively in normal group and Thy group. (P <0.01). The percentage of VSMCs contraction caused by α1A induced by Ca2 + influx was 47.7% ± 50% in the normal group and 21.2% ± 9.4% in the Thy group, respectively (P <0. 01). The percentage of contraction induced by intracellular calcium release after adding CPU 86 0 17 (30 μmol·L-1) was 35 2% ± 10 1% in the normal control group and 35 2% ± 10 2% in the Thy group The percentage of contraction induced by calcium influx was 13 9% ± 7 1% and 2 0 7% ± 7 5%, respectively. Conclusion L thyroxine enhances the effect of α1B and attenuates the effect of α1A. CPU 86 0 17 under normal circumstances the inhibition of α1A VSM stronger than α1B receptor subtype