Aizawa H, Inoue H, Koto H, Ikeda T, Hirose T
Research Institute for Diseases of the Chest, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1991 Nov;29(11):1425-31.
It has been reported that low concentrations of vasoactive intestinal peptide (VIP) suppress the release of acetylcholine (ACh) from vagal nerve terminals. However, there is little documentation of the neuro-effector transmission of VIP in human airways. In the present study, the effects of VIP on excitatory neuro-effector transmission in the human bronchus were investigated, in comparison with feline trachea. In feline trachea, VIP (10(-10) to 10(-7) M) reduced the amplitude of contractions evoked by field stimulation in the presence of indomethacin (10(-6) M). By contrast, VIP (10(-10) to 10(-9) M) had no effect on ACh-sensitivity of smooth muscle cells. These results indicate that VIP in low concentrations has a pre-junctional action inhibiting excitatory neuro-effector transmission, in addition to a post-synaptic action, presumably suppressing transmitter release from the vagal nerve terminals. On the other hand, in human bronchi, VIP (10(-9) to 10(-7) M) did not affect either contractions evoked by field stimulation or those evoked by ACh. These results indicate that VIP does not exhibit any pre-junctional effects in the human bronchus at these concentrations.
据报道，低浓度的血管活性肠肽（VIP）可抑制迷走神经末梢乙酰胆碱（ACh）的释放。然而，关于VIP在人类气道中的神经效应器传递的文献报道较少。在本研究中，与猫气管相比，研究了VIP对人支气管兴奋性神经效应器传递的影响。在猫气管中，在吲哚美辛（10^(-6) M）存在的情况下，VIP（10^(-10)至10^(-7) M）降低了场刺激诱发的收缩幅度。相比之下，VIP（10^(-10)至10^(-9) M）对平滑肌细胞的ACh敏感性没有影响。这些结果表明，低浓度的VIP除了具有突触后作用（可能抑制迷走神经末梢释放递质）外，还具有抑制兴奋性神经效应器传递的突触前作用。另一方面，在人支气管中，VIP（10^(-9)至10^(-7) M）既不影响场刺激诱发的收缩，也不影响ACh诱发的收缩。这些结果表明，在这些浓度下，VIP在人支气管中不表现出任何突触前效应。
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