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纸质出版:2011
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β2受体对心肌梗死大鼠心肌细胞钠钙交换电流调控[J]. 中山大学学报(医学科学版), 2011,32(4).
Signal Transduction Pathway of β2-Adrenergic Receptor Regulating INCX in Myocytes of Infarcted Rats[J]. Journal of Sun Yat-sen University (Medical Sciences), 2011, 32(4).
【目的】研究β肾上腺素受体(β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β受体激动剂salbutamolcAMP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】 β受体激动可能通过Gi-cAMP-PKA途径参与调节INCX
【Objective】 To investigate the signal transduction pathway of β-adrenergic receptor (β-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 -AR might regulate INCX through the pathway of Gi-cAMP-PKA.
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