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作 者:何可 肖慧 卢昊阳 代曼玉 沈兵[2] 赵韧[1] He Ke;Xiao Hui;Lu Haoyang(Dept of Cardiology,The First Affiliated Hospital of Anhui Medical University,Hefei 230022)
机构地区:[1]安徽医科大学第一附属医院心血管内科,合肥230022 [2]安徽医科大学基础医学院,合肥230022
出 处:《安徽医科大学学报》2021年第8期1263-1268,共6页Acta Universitatis Medicinalis Anhui
基 金:安徽高校自然科学研究项目(编号:KJ2014A122)。
摘 要:目的探讨不同浓度高盐环境下大鼠冠状动脉平滑肌中钙库操纵的钙内流(SOCE)及其介导的收缩功能的影响。方法不同浓度高盐培养基(分别含137.65~167.65 mmol/L NaCl)培养离体大鼠冠状动脉24 h后,采用免疫组化检测Orai1、STIM1、IP3R和ETA在冠状动脉平滑肌中表达情况;应用微血管张力测定系统检测U46619、ET-1和SOCE诱导的大鼠冠状动脉收缩功能;用钙成像技术检测RCASMCs中SOCE。结果高盐培养可显著增强ET-1和SOCE诱导的冠状动脉收缩(P<0.01)及RCASMCs中SOCE介导的Ca^(2+)内流(P<0.01),并使Orai1、STIM1、IP3R在冠状动脉平滑肌中表达显著上调(P<0.05)。结论细胞外高盐环境可增强激动剂及SOCE诱导的大鼠冠状动脉的收缩功能,其机制可能与平滑肌IP3受体-SOCE途径相关蛋白表达上调及SOCE介导的Ca^(2+)内流增强有关。Objective To investigate the effects of high-salt environment on store-operated calcium entry(SOCE)and contractile function in rat coronary artery smooth muscle.Methods After culturing the isolated rat coronary arteries in different concentrations of high-salt culture media(with 137.65~167.65 mmol/L NaCl respectively)for 24 h,the distribution and expression of Orai1,STIM1,IP3R and ETA in coronary artery smooth muscle were detected by immunohistochemistry assays,U46619,ET-1 and SOCE-induced coronary vasoconstriction were examined by microvascular tension measurement system,and the SOCE mediated Ca^(2+)influx in RCASMCs was detected by calcium imaging technology.Results High-salt environment significantly enhanced ET-1 and SOCE-induced coronary vasoconstriction(P<0.01)and SOCE mediated Ca^(2+)influx in the RCASMCs(P<0.01),and increased the expression of Orai1,STIM1 and IP3R in coronary artery smooth muscle(P<0.05).Conclusion The extracellular high-salt environment can enhance the contractile function of rat coronary artery induced by agonist and SOCE,and the mechanism may be associated with the up regulation of key proteins related to the IP3R-SOCE pathway and the enhancement of Ca^(2+)influx mediated by SOCE in the rat coronary artery smooth muscle.
关 键 词:高盐 冠状动脉 血管收缩 血管平滑肌 钙库操纵的钙内流
分 类 号:R331.5[医药卫生—人体生理学] R322.1[医药卫生—基础医学]
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