Canine pulmonary vasoreactivity to serotonin: role of protein kinase C and tyrosine kinase.
Canine pulmonary vasoreactivity to serotonin: role of protein kinase C and tyrosine kinase.
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犬肺血管对血清素的反应性：蛋白激酶 C 和酪氨酸激酶的作用。
DOI：
10.1152/ajpheart.1997.272.2.h740
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Isales,CM
中科院分区：
文献类型：
--
作者：
Barman,SA;Pauly,JR;Isales,CM
研究了蛋白激酶C和蛋白酪氨酸激酶介导的信号转导在犬肺血管对5-羟色胺（5-HT）反应中的作用。用血管闭塞技术测量肺血管阻力和顺应性。5-HT （10(-5) M）显着增加了约150%的毛细前阻力和两倍的毛细后阻力，并通过降低大血管顺应性和中室顺应性显着降低了总血管顺应性，约为控制值的50%。5- ht2受体阻滞剂酮色林（10(-7)M）、蛋白激酶C抑制剂staurosporine （10(-7) M）、电压依赖性Ca2+通道阻滞剂维拉帕米（10(-5)M）和特异性蛋白酪氨酸激酶抑制剂染料木素（5 × 10(-4) M）和tyrphostin 25 （5 × 10(-4) M）完全抑制了对5- ht的加压反应，而5- ht1受体拮抗剂pindolol （10(-7) M）对血清素能反应没有显著影响。这些结果表明，犬肺血管对5-HT的反应涉及5-HT2受体的激活，并表明这种受体信号转导途径涉及蛋白激酶C和酪氨酸激酶以及电压依赖性Ca2+通道的激活。
The role of protein kinase C- and protein tyrosine kinase-mediated signal transduction in the canine pulmonary vascular response to serotonin (5-HT) was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured with vascular occlusion techniques. 5-HT (10(-5) M) significantly increased precapillary resistance by approximately 150% and postcapillary resistance twofold and significantly decreased total vascular compliance to approximately 50% of control values by decreasing large-vessel compliance and middle-compartment compliance. The 5-HT2-receptor blocker ketanserin (10(-7) M), the protein kinase C inhibitor staurosporine (10(-7) M), the voltage-dependent Ca2+-channel blocker verapamil (10(-5) M), and the specific protein tyrosine kinase inhibitors genistein (5 x 10(-4) M) and tyrphostin 25 (5 x 10(-4) M) completely inhibited the pressor response to 5-HT, whereas the 5-HT1-receptor antagonist (-)pindolol (10(-7) M) had no significant effect on the serotonergic response. These results indicate that the canine pulmonary vascular response to 5-HT involves activation of 5-HT2 receptors and suggests that this receptor signal transduction pathway involves protein kinase C and tyrosine kinase and the activation of voltage-dependent Ca2+ channels.