Ellis J L, Conanan N D
Division of Clinical Immunology, John Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224-6801, USA.
Am J Respir Crit Care Med. 1996 Jul;154(1):244-6. doi: 10.1164/ajrccm.154.1.8680688.
The effect of prostaglandin E2 (PGE2) on cholinergic responses elicited by electrical field stimulation (EFS) (8 Hz, 1 ms, 8 V for 10 s every 100 s) of human isolated human bronchi was studied. Indomethacin (1 microM) was found to produce approximately a 100% increase in the cholinergic response. In the presence of indomethacin, PGE2 (1-300 nM) was found to concentration-dependently inhibit the cholinergic responses to EFS. A maximal inhibition was obtained with 100 nM PGE2 which produced an 80% inhibition of the cholinergic response. By contrast 100 nM PGE2 was without significant effect on the concentration response curve to exogenously added acetylcholine. The inhibitory effect of PGE2 on the EFS-induced cholinergic responses was not modified by the large conductance Ca(2+)-activated K+ channel inhibitor charybdotoxin (100 nM). These results suggest that endogenously released prostaglandins, presumably PGE2, act to inhibit cholinergic responses by a prejunctional mechanism in human isolated bronchi. In contrast to other autocoids, this inhibition does not involve the activation of large-conductance Ca(2+)-activated K+ channels.
研究了前列腺素E2（PGE2）对人离体支气管电场刺激（EFS）（8Hz，1ms，8V，每100秒刺激10秒）引发的胆碱能反应的影响。发现吲哚美辛（1μM）可使胆碱能反应增加约100%。在吲哚美辛存在的情况下，发现PGE2（1 - 300nM）浓度依赖性地抑制对EFS的胆碱能反应。100nM PGE2可产生最大抑制作用，使胆碱能反应抑制80%。相比之下，100nM PGE2对外源性添加乙酰胆碱的浓度反应曲线无显著影响。大电导钙激活钾通道抑制剂查卡毒素（100nM）未改变PGE2对EFS诱导的胆碱能反应的抑制作用。这些结果表明，内源性释放的前列腺素，可能是PGE2，通过人离体支气管中的节前机制来抑制胆碱能反应。与其他自体活性物质不同，这种抑制不涉及大电导钙激活钾通道的激活。
