Kv通道和ERK1/2在15-HETE引起缺氧肺动脉收缩中的作用  

Effect of 15-HETE-induced-vasoconstriction on hypoxic rat related to Kv channels and ERK1/2

作　　者：韩维娜[1] 庞彦喜 郭蕾[1] 朱大岭[1,3] 

机构地区：[1]哈尔滨医科大学药物化学与天然药物化学教研室,黑龙江哈尔滨150081 [2]山东高密卫生局,山东高密261500 [3]黑龙江省生物医药工程重点实验室,黑龙江哈尔滨150081

出　　处：《哈尔滨医科大学学报》2010年第2期129-132,共4页Journal of Harbin Medical University

基　　金：黑龙江省卫生厅课题(2007-478)

摘　　要：目的用组织浴槽血管环技术研究Kv通道和ERK1/2在15-HETE引起缺氧肺动脉收缩中的作用及其机制。方法游离缺氧Wistar大鼠的肺内肺动脉,直径约为0.5-1.0 mm,剪成长约3 mm的血管环,观察加入Kv通道抑制剂4-AP和ERK1/2抑制剂U0126前后15-HETE对大鼠离体肺动脉的作用。结果①MEK-ERK1/2阻断剂U0126可以明显阻断4-AP引起的肺动脉收缩（P〈0.05）;②Kv通道阻断剂4-AP可以明显阻断15-HETE引起的缺氧鼠肺动脉收缩（P〈0.05）;③U0126＋15HETE与U0126＋4-AP＋15HETE组之间有明显差异（P〈0.05）,Kv通道和ERK1/2均参与了15-HETE引起缺氧肺动脉收缩。结论15-HETE通过Kv通道引起缺氧肺动脉收缩,其机制可能与MEK-ERK1/2信号转导通路有关。Objective To investigate the effect and mechanism of 15-HETE-induced-vasoconstriction related to Kv channels and ERK1/2 on rat isolated pulmonary arterial rings.Methods Wistar rats weighing were anesthetized by sodium pentobarbital（40 mg/kg）.Pulmonary arteries（PA）were extracted and cut into rings（0.5～1.0 mm in diameter and 3 mm in length） for organ bath experiments.And we observed the role of 15-HETE-induced-vasoconstriction on isolated hypoxia rat pulmonary artery before and after adding Kv channel inhibitor 4-AP and ERK1/2 inhibitor U0126.Results ①Compared with the 4-AP group,U0126＋4-AP groups significantly reduced thecontraction of isolated hypoxic pulmonary artery rings（P〈0.05）.②Compared with the 15-HETE groups,4-AP＋15-HETE groups significantly reduced the contraction of isolated hypoxic rat＇s pulmonary artery rings（P〈0.05）,which is in the experimental results were consistent with hypoxic rabbit.③ Compared with the U0126＋15-HETE groups,U0126＋4-AP＋15-HETE groups significantly reduced the contraction of isolated hypoxic pulmonary artery rings（P〈0.05）.Conclusion 15-HETE-induced-vasoconstriction through the Kv channels in isolated hypoxic PA,which can relate to MEK-ERK1/2 signal transduction pathways.

关 键 词：15-羟基二十碳四烯酸 肺动脉环 4-氨基吡啶 细胞外信号调节激酶 

分 类 号：R332[医药卫生—人体生理学]