【摘要】 目的　观察ATP所引起的蟾蜍椎旁交感神经节细胞电位变化和有关因素的影响 ,以探讨ATP在神经节内的作用及其机制。方法　采用细胞外微电极技术记录离体灌流神经节电位。结果　外源性ATP(2 0 0 μmol L)可引起去极化 (n =1 1 0 ) ,超极化 (n =33) ,以及去极后伴随一超极过程的双相反应 (n =1 2 )。P2 嘌呤受体拮抗剂ci bacronblue 3GA(30 0 μmol/L)和奎尼丁 (30 0 μmol/L) ,均可抑制ATP所致去极反应 ,其幅值分别减小 (2 4 .2± 1 7.5 ) %(n =1 8,P <0 .0 1 )和 (32 .5± 1 1 .5 ) % (n =2 1 ,P <0 .0 1 )。P1 嘌呤受体拮抗剂氨茶碱 (2 0 0 μmol L) ,可抑制ATP所致超极反应 ,幅值减小 (6 5 .0± 2 2 .9) % (n =9,P <0 .0 1 )。在无钠溶液中 ,ATP的去极幅值变化为 (1 3.6± 1 7.5 ) % (n =1 0 ,P >0 .0 5 ) ,无统计学意义。在无钙溶液中或同时加用EDTA(1mol L)以去除溶液的Ca2 + ,可使ATP所致去极幅值减小 (2 3.6± 1 8.3) % (n =1 5 ,P <0 .0 1 )。电压依赖性钾通道阻断剂 4—氨基吡啶 (3mmol L)和ATP敏感性钾通道阻断剂格列苯脲 (1 0 0mol L) ,均可可抑制ATP所致超极反应 ,其幅值分别减小 (6 4 .5± 2 1 .9) % (n =1 1 ,P <0 .0 1 )和(6 6 .4± 2 2 .4 ) % (n =6 ,P <0 .0 1 )。前列腺素合成酶抑制剂吲更多还原

【Abstract】 Objective To investigate ATP induced potential and its effective variations resulted from certain factors observed for analyzing the mechanisms involved in it. Method Extracellular microelectroode technique was used to record the potential in superfused and isolated paravertebral sympathetic ganglion (PSG) of toad. Results Exogenous adenosine 5’ triphosphate(ATP, 200 μmol/L) induced a depolarization ( n =110), a hyperpolarization ( n =33) or a biphasic response forming with a depolarization followed by a hyperpolarization( n =12).P\-2 purinoceptor antagonists cibacron blue 3GA (300 μmol/L) and quinidine (300μmol/L) both depressed the ATP induced depolarization. The amplitudes of potential decreased by 24.2±17.5% (n=18, P<0.01) and 32.5±11.5% ( n =21, P<0. 01),respectively.P\-1 purinoceptor antagonist aminophylline (200 μmol/L)depressed the ATP induced hyperpolarization, the amplitude decreased by 65.0 ±22.9% ( n =9, p<0.01). In the Na\++ free perfusate, the variation of depolarization amplitude was 13.6±17.5%( n =10, P>0.05), without statistical significance.In the Ca\+\{2+\} free solution or coexisting with EDTA (1.0 mmol/L) to remove Ca\+\{2+\},ATP induced depolarization decreased by 23.6±18.3%( n =15, P<0. 01).Voltage dependent k + channel blocker 4 aminopyridine(3 mmol/L) and ATP sensitive K\++ channel blocker glibenclamide (100 μmol/L) both depressed the ATP induced hyperpolarization, its amplitudes decreased by 64 5±21 9% ( n =11, P<0 01) and 66.4±22.4% ( n =6,P<0. 01),respectively. Prostaglandin synthetase inhibitor indomethacin (500μmol/L) depressed ATP induced depolarization, its amplitude decreased by 66.4±12.8% ( n =8, P<0.01).Exogenous cAMP (400 μmol/L) could mimic the ATP induced hyperpolarization in the PSG( n =8). Conclusion There exist P\-1 and P\-2 purinoceptors in the PSG of toad. Both of them can mediate the ATP induced depolarization. P\-2 purinoceptor also mediates the ATP induced hyperpolarization. Ca\+\{2+\} and K\++ are probably the main carriers of charge in ATP induced depolarizing and hyperpolarizing response, respectively. The messenger for mediating these two kinds of responses may be prostaglandin and cAMP ,respectively.更多还原