K物质对大鼠心肌细胞收缩的影响及其信号传导通路的探讨

Signal transduction pathway for cardiac myocyte contraction induced by Substance K in rats

目的 研究K物质引起大鼠心肌细胞收缩的信号传导通路。方法 应用钙离子荧光指示剂Fluo 3AM负载原代培养的大鼠心肌细胞 ,通过流式细胞仪检测心肌细胞内游离钙离子浓度 ( [Ca2 + ]i)变化 ;分别应用磷脂酶C抑制剂 新霉素 ,三磷酸肌醇受体拮抗剂 肝素阻断肌醇磷脂 钙信号系统 ,观察二者对K物质诱导的 [Ca2 + ]i变化的影响。结果 SK( 1.78× 10 -5mol/L)能升高 [Ca2 + ]i,新霉素、肝素均可阻断SK诱导的 [Ca2 + ]i升高的效应。结论 SK可升高心肌细胞[Ca2 + ]i,其作用与肌醇磷脂

Objective To study the signal transduction pathway for myocyte contraction induced by Substance K (SK) in rats. Methods The fluorescent Ca 2+ indicator Fluo 3AM was used to quantitate the calcium signal directly in the primary cultured myocardial cells. Changes of free Ca 2+ concentration in cardiac myocytes were detected by flow cytometry. The phospholipase C (PLC) inhibitor, neomycin and IP3 receptor antagonist, heparin, were used to block signal system of phosphates Ca 2+ in order to investigate whether they took part in the SK induced changes of [Ca 2+ ]i in myocytes. Results SK(1.78×10 -5 mol/L) elevated [Ca 2+ ]i in myocytes. The effects could be blocked by neomycin and heparin. Conclusion SK can elevate [Ca 2+ ]i in myocyte, which may be mediated by a signal system of phosphates Ca 2+ .