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目的 探讨酪氨酸激酶在Ca2 +池操纵性Ca2 +内流中的作用。方法 记录大鼠胸主动脉环收缩反应。结果 ①不同剂量酪氨酸激酶抑制剂 genistein (1～ 10 0 μmol·L-1)和tyrphostin 2 5 (Tyr 2 5 ,1～ 30 μmol·L-1)均以浓度依赖性抑制cyclopiazonicacid (CPA)引起的平滑肌收缩平台期。Tyr 2 5的最大作用浓度为 10 μmol·L-1,抑制率为 42 %±11%。② 10 μmol·L-1Tyr 2 5和 1μmol·L-1nifedipine(Nif)对CPA引起电压依赖性Ca2 +通道 (VDCC)开放过程的抑制作用存在部分交叉。③ 1μmol·L-1Nif预处理阻断VDCC作用后 ,10 μmol·L-1Tyr 2 5只能部分阻断CPA引起的Ca2 +池操纵性Ca2 +通道 (SOCC)开放过程 ,再加入 6 0 μmol·L-1SK&F96 36 5可完全阻断SOCC的开放过程。结论 CPA引起平滑肌的收缩过程中 ,蛋白质酪氨酸激酶参与了开启VDCC和SOCC的信号转导过程
Objective To investigate the role of tyrosine kinases in Ca2 + influx in Ca2 + pool. Methods The thoracic aortic rings were recorded. Results ① Tyrosine kinase inhibitor genistein (1 ~ 100 μmol·L -1) and tyrphostin 2 5 (Tyr 2 5, 1 ~ 30 μmol·L -1) inhibited cyclopiazonic acid (CPA) in a dose- Induced smooth muscle contraction platform. The maximum concentration of Tyr 2 5 was 10 μmol·L-1 and the inhibition rate was 42% ± 11%. ② The inhibitory effect of 10 μmol·L-1Tyr 2 5 and 1 μmol·L-1nifedipine (Nif) on the opening of voltage-dependent Ca 2+ channel (VDCC) induced by CPA was partly cross-linked. ③ After pretreatment with 1μmol·L-1Nif, the effect of 10μmol·L-1Tyr 2 5 partially blocked the Ca2 + pool Ca 2+ channel (SOCC) opening induced by CPA, and then added 60μmol · L L-1SK & F96 36 5 can completely block the open process of SOCC. CONCLUSIONS: During CPA-induced contractions of smooth muscle, protein tyrosine kinases are involved in the signal transduction that turns on VDCC and SOCC