The properties of junction potentials evoked by nerve stimulation and by local application of drugs, and currents evoked by nerve stimulation, in the smooth muscle cells of the guinea-pig vas deferens have been investigated. The effects of temperature on these responses have been studied using intracellular and extracellular recording. 2. Local, brief (5-15 ms) application of 10(-4) M-adenosine-5'-triphosphate (ATP) from glass micropipettes onto the surface of the vas deferens, using pressure pulses (103-206 kPa), elicited a depolarization of the smooth muscle cell membranes which closely resembled the nerve stimulation-evoked excitatory junction potential (EJP). 3. Local application of 10(-4) M-noradrenaline (NA) failed to produce any detectable membrane potential response. Junction potentials elicited by a mixture of 10(-4) M-ATP and 10(-4) M-NA (ratio by volume 1:50) in the drug ejection micropipette were similar in shape to those evoked by ATP alone. 4. Cooling the tissue from 35 to 25 degrees C did not significantly alter resting membrane potentials but resulted in a significant prolongation of the rising and decaying phases of the EJPs. Fifty per cent decay times for EJPs at 35 and 25 degrees C were (mean +/- S.D.) 236 +/- 20 and 434 +/- 30 ms respectively (P less than 0.01). 5. Extracellularly recorded excitatory junction currents (EJCs) elicited by nerve stimulation, believed to reflect the transmembrane current underlying the EJPs, were prolonged in parallel at low temperatures (50% decay times of EJCs at 35 and 25 degrees C: 11.73 +/- 3.94 and 26.15 +/- 8.4 ms, respectively, P less than 0.01). 6. Junction potentials evoked by locally applied, exogenous ATP were also significantly prolonged by cooling (50% decay times: 663 +/- 88 ms at 35 degrees C and 1955 +/- 79 ms at 25 degrees C, P less than 0.01). 7. Bath application of 10(-6) M-alpha,beta-methylene ATP, the enzymatically stable, desensitizing analogue of ATP, reversibly abolished nerve-evoked EJPs. Local application of 10(-6) M-alpha,beta-methylene ATP led to a prolonged depolarization of the smooth muscle cells lasting between 20 and 60 s. 8. Junction potentials elicited by locally applied alpha,beta-methylene ATP were not prolonged or otherwise significantly altered on cooling. The durations of the depolarizations were 46.0 +/- 12.1 s at 35 degrees C and 43.4 +/- 10.6 s at 25 degrees C (P greater than 0.1).(ABSTRACT TRUNCATED AT 400 WORDS)
摘要
对豚鼠输精管平滑肌细胞中神经刺激诱发的结电位、药物局部应用诱发的结电位以及神经刺激诱发的电流的特性进行了研究。使用细胞内和细胞外记录研究了温度对这些反应的影响。2. 使用压力脉冲（103 - 206 kPa），从玻璃微吸管将10⁻⁴ M - 腺苷 - 5'-三磷酸（ATP）局部、短暂（5 - 15毫秒）施加到输精管表面，引发平滑肌细胞膜去极化，这与神经刺激诱发的兴奋性结电位（EJP）非常相似。3. 局部应用10⁻⁴ M - 去甲肾上腺素（NA）未能产生任何可检测到的膜电位反应。药物喷射微吸管中10⁻⁴ M - ATP和10⁻⁴ M - NA（体积比1:50）混合物诱发的结电位形状与单独ATP诱发的相似。4. 将组织温度从35℃冷却至25℃不会显著改变静息膜电位，但导致EJP上升和衰减阶段显著延长。35℃和25℃时EJP的50%衰减时间分别为（平均值±标准差）236±20毫秒和434±30毫秒（P＜0.01）。5. 神经刺激诱发的细胞外记录的兴奋性结电流（EJC），被认为反映了EJP背后的跨膜电流，在低温下也平行延长（35℃和25℃时EJC的50%衰减时间分别为：11.73±3.94毫秒和26.15±8.4毫秒，P＜0.01）。6. 局部应用外源性ATP诱发的结电位也因冷却而显著延长（50%衰减时间：35℃时为663±88毫秒，25℃时为1955±79毫秒，P＜0.01）。7. 浴槽中加入10⁻⁶ M - α,β - 亚甲基ATP，这是一种酶稳定、脱敏的ATP类似物，可逆地消除神经诱发的EJP。局部应用10⁻⁶ M - α,β - 亚甲基ATP导致平滑肌细胞去极化延长，持续20至六十秒。8. 局部应用α,β - 亚甲基ATP诱发的结电位在冷却时没有延长或其他显著改变。去极化持续时间在35℃时为46.0±12.1秒，在25℃时为43.4±10.6秒（P＞0.1）。（摘要截断于400字）
