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目的:研究腺苷三磷酸(ATP)对兔离体窦房结起搏细胞动作电位的作用,分析相关受体。方法:利用细胞内微电极技术记录兔离体窦房结细胞跨膜电位。结果:ATP 0.1-3.0mmol/L浓度依赖性减慢窦房结自发搏动速率16％-43％,降低舒张期除极速率33％-67％,增大动作电位幅值6％9％,加快最大除极速率30％-76％,APD_(50)和APD_(90)分别缩短7％-12％和6.3％-9％,等浓度ATP、腺苷二磷酸(ADP)和腺苷(Ado)的效应相比时,各组间无显著性差异,尿苷三磷酸(UTP)和α,β-meATP对动作电位各参数均无影响,P1受体拮抗剂氨茶碱(0.1mmol/L)显著拮抗ATP和Ado的作用(P<0.05),且拮抗程度相同,P2受体拮抗剂反应兰2 (0.05mmol/L)不影响ATP的作用(P<0.05)。结论:兔窦房结不存在功能性P2X,和P2Y_2受体,ATP对兔窦房结的作用主要通过其降解产物Ado,由P1受体介导而发挥。
Objective: To study the effect of adenosine triphosphate (ATP) on the action potentials of pacemaker cells isolated from isolated sinus node in rabbits and to analyze the related receptors. Methods: The transmembrane potential of isolated sinoatrial node cells was recorded by intracellular microelectrode technique. Results: ATP 0.1-3.0mmol / L slowed the spontaneous pulsatile rate of sinoatrial node by 16% -43% in a concentration-dependent manner, decreased the diastolic depolarization rate by 33% -67% and increased the action potential amplitude by 6% -9% APD_ (50) and APD_ (90) were reduced by 7% -12% and 6.3% -9%, respectively, with the same depolarization rate of 30% -76%, ATP, ADP and Ado, (UTP) and α, β-meATP had no effect on the parameters of action potentials. P1 receptor antagonist aminophylline (0.1 mmol / L) (P <0.05), and antagonized to the same extent. P2 receptor antagonist Reactive Blue 2 (0.05 mmol / L) did not affect the effect of ATP (P <0.05). CONCLUSION: Functional P2X and P2Y_2 receptors are absent in rabbit sinoatrial node. The effect of ATP on rabbit sinoatrial node is mainly mediated by P1 receptor through its degradation product Ado.