【摘要】 【目的】研究β2肾上腺素受体(β2受体)对心肌梗死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30只,随机分为正常对照和心肌梗死(MI)组,制作MI模型。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INCX,予以β2受体激动剂salbutamol、cAMP激动剂forskolin、抑制性cAMP类似物Rp-cAMPS、PKA抑制剂H89及Gi蛋白抑制剂后记录INCX的变化。【结果】在正常和梗死后4周心肌细胞,forskolin可使INCX电流密度升高108.9%和70.3%(P<0.05),抑制性cAMP类似物Rp-cAMPS可抑制salbutamol升高INCX电流密度的作用(P<0.05),PTX能增大salbutamol的作用,INCX电流密度较单独予以salbutamol升高36.8%和50.6%(P<0.05),H89可抑制salbutamol升高INCX电流密度的作用(P<0.05)。【结论】β2受体激动可能通过Gi-cAMP-PKA途径参与调节INCX。更多还原

【Abstract】 [Objective] To investigate the signal transduction pathway of β2-adrenergic receptor(β2-AR) regulating INCX in myocytes from infarcted rats.[Methods] Thirty adult Wistar rats were divided into two groups at random:the control group(n = 15) and the post-myocardial infarction(post-MI) group(n = 15).The chest of rats were opened and ligature were placed around the left anterior descending coronary artery.Rats in control group were sham-operated without coronary artery ligation.Myocytes were enzymatically disassociated by Langedorff 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.[Results] In the control group and the post-MI group,treatment with forskolin increased inward INCX in ventricular myocytes by 108.9% and 70.3%(P < 0.05),respectively.An inhibitory cAMP analog(Rp-cAMPS) and H89 attenuated the rise of INCX induced by salbutamol(a selective beta2-AR agonist)(P < 0.05);pertussis toxin enlarged the rise of INCX by 36.8% and 50.6%(P < 0.05),respectively.[Conclusion] Beta 2-AR might regulate INCX through the pathway of Gi-cAMP-PKA.更多还原