Ito Y, Tajima K
J Physiol. 1981;319:379-92. doi: 10.1113/jphysiol.1981.sp013915.
Neuro-effector transmission in the smooth muscle layer of the dog trachea was studied in vitro using the micro-electrode and double sucrose gap methods.1. Electrical field stimulations with short duration (50-100 musec) applied to the whole tissue produced an excitation of the intrinsic nerves, and evoked excitatory junction potentials (e.j.p.s) followed by twitch tension development and subsequent long lasting relaxation of the smooth muscle tissue.2. The effects of field stimulations were abolished by tetrodotoxin (2 x 10(-7)m), and atropine (1.7 x 10(-5)m) selectively blocked both the e.j.p. and twitch tension. On the other hand, propranolol (1.9 x 10(-5)m) suppressed the generation of the prolonged relaxation evoked by the field stimulations.3. E.j.p.s recorded by the double sucrose gap method showed gradual and continuous reduction in amplitude during prolonged exposure in Krebs solution (1-2 hr), and there were no changes in the membrane potential or in the input membrane resistance.4. With application of indomethacin (10(-5)m), a gradual and continuous reduction in the amplitude of e.j.p. was no longer observed, and (after the initial increase in the amplitude) e.j.p.s with a constant amplitude were obtained during 1-1.5 hr. Indomethacin (10(-5)m) modified neither the resting membrane potential nor the input membrane resistance of smooth muscle cells.5. After pre-treatment with indomethacin, low concentrations (10(-11)-10(-8)m) of prostaglandin E(1) or E(2) (PGE series) markedly suppressed the amplitude of e.j.p. with no changes in the resting membrane potential or in the input membrane resistance.6. During the repetitive field stimulation at the stimulus frequency of 0.1-1 Hz, the amplitude of the e.j.p.s was gradually reduced (the depression process). The depression was not affected by applications of prostaglandins, indomethacin or alpha- and beta-adrenoceptor blockers.7. These results indicate that in the dog tracheal smooth muscles, the endogenous PGE series may play an important role in feed-back inhibitory mechanisms, at the nerve terminals related to acetylcholine release.
采用微电极和双蔗糖间隙法在体外研究了犬气管平滑肌层的神经效应器传递。
对整个组织施加短持续时间（50 - 100微秒）的电场刺激可激发内在神经，诱发兴奋性接头电位（e.j.p.s），随后出现平滑肌组织的抽搐张力发展及随后的持久松弛。
河豚毒素（2×10⁻⁷m）可消除电场刺激的效应，阿托品（1.7×10⁻⁵m）选择性地阻断e.j.p.和抽搐张力。另一方面，普萘洛尔（1.9×10⁻⁵m）抑制电场刺激诱发的持久松弛的产生。
用双蔗糖间隙法记录的e.j.p.s在Krebs溶液中长时间暴露（1 - 2小时）期间，其幅度逐渐持续降低，膜电位或输入膜电阻无变化。
应用吲哚美辛（10⁻⁵m）后，不再观察到e.j.p.幅度的逐渐持续降低，并且（在幅度最初增加后）在1 - 1.5小时内获得了幅度恒定的e.j.p.s。吲哚美辛（10⁻⁵m）既不改变平滑肌细胞的静息膜电位也不改变输入膜电阻。
用吲哚美辛预处理后，低浓度（10⁻¹¹ - 10⁻⁸m）的前列腺素E₁或E₂（PGE系列）显著抑制e.j.p.的幅度，而静息膜电位或输入膜电阻无变化。
在0.1 - 1Hz的刺激频率下进行重复电场刺激期间，e.j.p.s的幅度逐渐降低（抑制过程）。该抑制不受前列腺素、吲哚美辛或α和β肾上腺素能受体阻滞剂应用的影响。
这些结果表明，在犬气管平滑肌中，内源性PGE系列可能在与乙酰胆碱释放相关的神经末梢的反馈抑制机制中起重要作用。
