血管平滑肌钙动员和钙敏感机制在高血压中的改变  

Changes of calcium mobilization and calcium-sensitization mechanism in vascular smooth muscle cells in hypertension

作　　者：汪燕[1] 周慧轩[1] 王莉[1] 

机构地区：[1]上海交通大学附属第六人民医院麻醉科,上海200233

出　　处：《中国药理学通报》2014年第2期287-291,共5页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 30972842)

摘　　要：血管张力受血管平滑肌(vascular smooth muscle,VSM)收缩水平的调控,是调节外周血管阻力和血压的重要因素。血管激动剂通过细胞内信号转导通路影响肌球蛋白轻链(myosin light chain20,MLC20)磷酸化水平,从而调节VSM的收缩。而MLC20磷酸化水平主要受肌球蛋白轻链激酶(myosin light chain kinase,MLCK)和肌球蛋白轻链磷酸酶(myosin light chain phosphatase,MLCP)的双向调节。前者与细胞内Ca2+浓度有关,后者取决于肌丝对Ca2+敏感性。原发性高血压中Ca2+动员和肌丝Ca2+敏感性增强,导致VSM过度收缩,是高血压重要的病理生理改变之一。所以,对血管平滑肌细胞(vascular smooth muscle cell,VSMC)钙动员和钙敏感机制在高血压中的改变进行研究可为原发性高血压的治疗提供新思路和新靶点。该文就VSMC钙动员和钙敏感机制在原发性高血压中的改变及其发病机制进行阐述。Vascular tone, which is an important determinant of peripheral vascular resistance and blood pressure, is affected by vascular smooth muscle （ VSM ） contraction. Stimulating factors may change the level of phosphorylation of myosin light chain （MLC20） , which is bidirectionally regulated by myosin light chain kinase （MLCK） and myosin light chain phosphatase （ ML- CP）. MLCK is related to the concentration of calcium in vascu-lar smooth muscle cells, while MLCP depends on myofilament sensitivity to calcium. In essential hypertension, both the calci-um mobilization and myofilament sensitivity to calcium have in-hanced, which results in hyper-contraction of vascular smooth muscle. It is one of the important pathogenesis of essential hy- pertension, which is becoming a new therapeutic target recently. In this paper, the changes of calcium mobilization and calcium sensitization in vascular smooth muscle cell and its mechanism inhypertension are reviewed.

关 键 词：高血压 血管平滑肌细胞 钙离子内流 钙离子释放 蛋白激酶C Rho相关激酶 

分 类 号：R322.12[医药卫生—人体解剖和组织胚胎学] R322.74[医药卫生—基础医学]