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TRPV4在高血压小鼠胸主动脉舒张中的作用
引用本文:阚昊,毛爱琴,张卡,张鹏,马鑫. TRPV4在高血压小鼠胸主动脉舒张中的作用[J]. 蚌埠医学院学报, 2018, 43(10): 1318-1321. DOI: 10.13898/j.cnki.issn.1000-2200.2018.10.013
作者姓名:阚昊  毛爱琴  张卡  张鹏  马鑫
作者单位:1. 江南大学 药学院, 江苏 无锡 214122;2. 无锡医学院, 江苏 无锡 214000
摘    要:目的:研究瞬时受体电位香草素亚型4(transient receptor potential vanilloid type 4,TRPV4)在高血压小鼠胸主动脉舒张中的作用,并探讨其作用机制。方法:分离小鼠胸主动脉,取其离体胸主动脉血管环进行血管张力测试,以1 μmol/L盐酸苯肾上腺素预收缩血管,分别观察对照组与TRPV4抑制剂HC067064处理组在乙酰胆碱(ACh)和GSK1016790A介导下血管张力变化,野生型与TRPV4基因敲除(TRPV4-/-)小鼠在ACh和GSK1016790A介导下血管张力变化;对于普通饮食组和高盐饮食组小鼠胸主动脉环进行血管张力测试,检测GSK1016970A舒张血管的张力变化。结果:HC067064组在ACh和GSK1016790A引起的动脉舒张反应明显低于对照组(P<0.05);TRPV4-/-小鼠胸主动脉环在ACh和GSK1016790A引起的动脉舒张反应亦低于野生型小鼠(P<0.05);高盐饮食组GSK1016790A引起的动脉舒张反应低于普通饮食组(P<0.05)。结论:TRPV4参与了小鼠胸主动脉的舒张作用,此作用是通过刺激TRPV4通道开放,促进内皮细胞外钙离子内流进入胞内,经过一系列信号转导,继而舒张血管;但是在病理模型,如高盐饮食下,TRPV4在胸主动脉中的舒张作用会被抑制。

关 键 词:TRPV4   高血压   胸主动脉   血管舒张
收稿时间:2018-07-31

Effect of TRPV4 in the diastole of thoracic aorta in hypertensive mice
Affiliation:1. School of Pharmaceutical Sciences, Jiangnan University, Wuxi Jiangsu 214122;2. Wuxi School of Medicine, Wuxi Jiangsu 214000, China
Abstract:Objective:To investigate the role of transient receptor potential vanilloid type 4(TRPV4) in the diastole of thoracic aorta in hypertensive mice,and explore its mechanism.Methods:The vascular tension of thoracic aorta in mouse was measured.The vasoconstriction was pre-contracted with 1 μmol/L phenylephrine hydrochloride(Phe).The vascular tension changes mediated by ACh and GSK1016790A in control group and TRPV4 inhibitor HC067064 treating group were observed,and the vascular tension changes mediated by ACh and GSK1016790A in wild type and TRPV4 knockout(TRPV4-/-) mice were observed.The vascular tension of the thoracic aorta rings in normal diet group and high salt diet group were measured to detect the vascular tension change induced by GSK1016970A.Results:The arterial diastole response induced by ACh and GSK1016790A in HC067064 group was significantly lower than that in control group(P<0.05).The arterial diastole response induced by ACh and GSK1016790A in thoracic aorta rings of TRPV4-/-mice was lower than that in wildtype mice(P<0.05).The arterial diastole response induced by GSK1016790A in high salt diet group was lower than that in normal diet group(P<0.05).Conclusions:TRPV4 is involved in the diastole of the thoracic aorta in mice.The action mechanism is to stimulate the opening of the TRPV4 channel,promote the extracellular calcium ion influx into the intracellular,and relax the blood vessels after a series of signal transduction.But for the pathological models,such as highsalt diet,the relaxation of TRPV4 in thoracic aorta can be inhibited.
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