Coleman R A, Levy G P
Br J Pharmacol. 1974 Oct;52(2):167-74. doi: 10.1111/j.1476-5381.1974.tb09697.x.
1 Electrical stimulation of the guinea-pig isolated tracheal tube causes a biphasic response, initially excitatory and then inhibitory. The excitatory response was abolished by atropine leaving the inhibitory response unaffected.2 The inhibitory response was greatly reduced but not abolished by propranolol or guanethidine. A residual inhibitory response was still present in tracheas in which sympathetic nerve function had been abolished by pretreatment with syrosingopine or 6-hydroxydopamine. These results show that the inhibitory response is predominantly adrenergic but that a small non-adrenergic component is also present.3 The non-adrenergic inhibitory response was abolished by lignocaine and tetrodotoxin suggesting that it is nervous in origin.4 Optimal stimulation parameters for the predominantly adrenergic inhibitory response were a pulse width of 0.7-2 ms, a stimulation period of 7 s and a frequency of 20 Hz. For the non-adrenergic inhibitory response, optimal stimulation parameters were a pulse width of 2 ms, a stimulation period of 12 s and a frequency of 20 Hz.5 Evidence obtained with pharmacological antagonists, enzyme inhibitors and activators suggested that the transmitter mediating the non-adrenergic inhibitory nervous response is unlikely to be: acetylcholine, histamine, 5-hydroxytryptamine, cyclic 3',5'-adenosine monophosphate or a prostaglandin.6 The adenosine uptake blocking drugs dipyridamole, hexobendine and Dilazep potentiated the non-adrenergic inhibitory nervous response and unmasked inhibitory responses to adenosine and adenosine 5'-triphosphate.7 It is concluded that electrical stimulation of the guinea-pig trachea, in addition to activating cholinergic and adrenergic nervous pathways, may activate a separate and distinct inhibitory nervous pathway. This pathway has some features in common with the non-adrenergic non-cholinergic inhibitory pathways in gastro-intestinal muscle.
对豚鼠离体气管进行电刺激会引起双相反应，最初是兴奋，随后是抑制。阿托品可消除兴奋反应，而抑制反应不受影响。
普萘洛尔或胍乙啶可使抑制反应大幅减弱，但并未消除。在用蛇根碱或6 - 羟基多巴胺预处理使交感神经功能被消除的气管中，仍存在残余的抑制反应。这些结果表明，抑制反应主要是肾上腺素能的，但也存在一小部分非肾上腺素能成分。
利多卡因和河豚毒素可消除非肾上腺素能抑制反应，提示其起源于神经。
主要肾上腺素能抑制反应的最佳刺激参数为：脉冲宽度0.7 - 2毫秒、刺激时长7秒、频率20赫兹。对于非肾上腺素能抑制反应，最佳刺激参数为：脉冲宽度2毫秒、刺激时长12秒、频率20赫兹。
药理学拮抗剂、酶抑制剂和激活剂的实验证据表明，介导非肾上腺素能抑制性神经反应的递质不太可能是：乙酰胆碱、组胺、5 - 羟色胺、环磷腺苷或前列腺素。
腺苷摄取阻断药物双嘧达莫、己酮可可碱和地拉卓可增强非肾上腺素能抑制性神经反应，并使对腺苷和三磷酸腺苷的抑制反应显现出来。
得出的结论是，对豚鼠气管进行电刺激，除了激活胆碱能和肾上腺素能神经通路外，可能还激活了一条独立且不同的抑制性神经通路。这条通路与胃肠道肌肉中的非肾上腺素能非胆碱能抑制通路有一些共同特征。
