摘要
目的研究血管内皮细胞(VEC)钙激活钾通道(KCa)在高糖所致内皮源性超极化因子(EDHF)介导的内皮舒张功能障碍中的作用。方法采用离体血管张力实验,观察高糖孵育大鼠肠系膜三级动脉3h后,IKCa和SKCa在EDHF介导的内皮舒张功能变化中的作用;采用Western blot技术,观察高糖孵育人脐静脉内皮细胞(HUVEC)48h对KCa3.1和KCa2.3蛋白表达的影响。结果 30mmol/L葡萄糖孵育大鼠肠系膜三级动脉3h可显著降低乙酰胆碱(ACh)诱导的内皮舒张反应、EDHF介导的内皮舒张反应及IKCa和SKCa介导的EDHF舒张反应。30mmol/L葡萄糖孵育HUVEC 48h显著降低KCa3.1和KCa2.3通道蛋白表达。而渗透压对照组30mmol/L甘露醇孵育大鼠肠系膜三级动脉和HUVEC对上述指标无明显影响。结论高糖损伤大鼠肠系膜三级动脉EDHF介导的内皮舒张功能,其机制与降低血管内皮细胞上KCa的表达和功能有关。
Objective To investigate the role of endothelial calcium-activated potassium channels in endothelium-derived hyperpolarizing factor （EDHF）-mediated endothelial diastolic dysfunction induced by high glucose. Methods The changes of ACh-induced vasodilatation mediated by IKCa and SKCa in mesentery arterioles of rats incubated with high glucose （mannitol as control） for 3 hours were measured by multi-myograph system. The protein levels of KCa3.1 and KCa2.3 in cultured human umbilical vein endothelial cells （HUVECs） were detected by Western blot. Results The vasodilatation mediated by EDHF, IKCa and SKCa was impaired in 30mmol/L glucose-incubated mesentery arterioles, but not in 30mmol/L mannitol-incubated ones. Incubation with 30mmol/L glucose for 48 hours significantly decreased the protein expression of KCa3.1 and KCa2.3. Conclusion High glucose impairs EDHF-mediated relaxation, which may be related to the down-regulation of KCa channels.
出处
《西安交通大学学报（医学版）》
CAS
CSCD
北大核心
2013年第5期609-613,共5页
Journal of Xi’an Jiaotong University（Medical Sciences）
基金
国家自然科学基金资助项目(No.81100231
81170137)
陕西省自然科学基金资助项目(No.2011JQ4021)~~
