Specific role of tyrosine kinase in the vascular contraction produced by stretch.

为了确定蛋白酪氨酸激酶机制是否参与压力性收缩，我们比较了三种结构无关的酪氨酸激酶抑制剂和酪氨酸磷酸酶抑制剂正钒酸盐对大鼠离体大脑后动脉压力性收缩的影响。用宽度分析仪连续测量血管直径的变化。Herbimycin A对压力诱导的收缩有抑制作用，而对氯化钾或9,11二脱氧-11 α， 9 α -环氧甲烷前列腺素f2 α (U46619)产生的收缩只有轻微的抑制作用。染料木素不仅能抑制压力诱导的收缩，还能抑制u46619诱导的收缩。Tyrphostin 23在压力、氯化钾和U46619三种不同刺激下显著减弱收缩。正钒酸盐增强了压力诱导的收缩。这些结果表明，herbyycin A是压力性收缩最特异性和最有效的抑制剂，蛋白质酪氨酸激酶机制可能在大鼠大脑动脉压力性收缩的发生中起重要作用。

In order to determine whether protein tyrosine kinase mechanisms are involved in pressure-induced contraction, we compared effects of three structurally-unrelated tyrosine kinase inhibitors and orthovanadate, a tyrosine phosphatase inhibitor, on the pressure-induced contraction of the posterior cerebral artery isolated from rats. The change in vessel diameter was continuously measured with a width analyzer. Herbimycin A inhibited the pressure-induced contraction, while it only slightly inhibited contractions produced by potassium chloride or 9,11 dideoxy-11alpha, 9alpha-epoxymethano prostaglandin F2alpha (U46619). Genistein inhibited not only the pressure-induced contraction but also the U46619-induced one. Tyrphostin 23 significantly attenuated contractions in response to three different stimuli, i.e., pressure, potassium chloride, and U46619. Orthovanadate potentiated the pressure-induced contraction. These results suggest that herbimycin A is the most specific and potent inhibitor of the pressure-induced contraction and that a protein tyrosine kinase machanism may play an important role in the genesis of the pressure-induced contraction of the rat cerebral artery.