β_2肾上腺素受体对心肌细胞钠钙交换电流调控的信号转导途径  

The signal transduction pathway of β_2-adrenergic receptor regulating INCX in myocytes

作　　者：杨蕙[1] 伍卫[2] 邓春玉[3] 

机构地区：[1]广州市第一人民医院鹤洞分院心内科,广东广州510380 [2]中山大学附属第五医院 [3]广东省人民医院心血管病研究所膜片嵌室

出　　处：《中国心脏起搏与心电生理杂志》2011年第4期343-345,共3页Chinese Journal of Cardiac Pacing and Electrophysiology

基　　金：广东省医学科学技术研究基金资助项目(项目编号:A2007494)

摘　　要：目的研究β2肾上腺素受体(β2受体)对大鼠心肌细胞钠钙交换电流(INCX)调控作用的信号转导途径。方法雄性健康Wistar大鼠12只,采用经典的酶分离心肌细胞方法,应用全细胞膜片钳技术记录给药前后INCX。药物组合方案包括:予以环磷酸腺苷(cAMP)激动剂forskolin灌流;灌流β2受体激动剂salbutamol后再以PKA(蛋白激酶A)抑制剂H89或抑制型G蛋白(Gi)抑制剂百日咳毒素(PTX)灌流。结果 forskolin可使INCX密度升高102.1%,H89可抑制salbutamol升高INCX密度的作用达34.7%,PTX能增大salbutamol的作用,INCX密度较单独予以salbutamol升高36.8%(P均<0.05)。结论β2受体激动可能通过刺激型G蛋白/Gi蛋白(Gi)-cAMP-PKA途径参与调节INCX。Objective To investigate the signal transduetion pathway of β2-adrenergic receptor（β2-AR） regulating INCX in myocytes. Methods Myocytes of twelve adult Wistar rats were enzymatically disassociated by Langedofff perfusion. Whole cell-patch clamp recording technique was used to record INCx in specific pipette solution and superfusion according to specific holding potential and command potential program. The response to forskolin and the β2-AR agonist salbutamol was obtained solely or after treatment with H89 or pertussis toxin（PTX）. Results Treatment with forskolin increased inward INCX in ventricular myocytes by 102.1% （P 〈 0. 05 ）. H89 attenuated the rise of INCx induced by salbutamol （P 〈 0. 05 ）. PTX enlarged the rise of INCX by 36.8% （P 〈 0.05 ）. Conclusion INCX might be regulated by β2-AR through the pathway of Gs/Gi-cAMP-PKA.

关 键 词：心血管病学 Β2肾上腺素受体 钠钙交换电流 信号转导 全细胞膜片钳技术 

分 类 号：R331.38[医药卫生—人体生理学]