Dey R D, Mayer B, Said S I
Department of Anatomy, West Virginia University, Morgantown 26506-9128.
Neuroscience. 1993 Jun;54(4):839-43. doi: 10.1016/0306-4522(93)90578-4.
Neurally-mediated relaxation of smooth muscle in human, guinea-pig, cat, and pig airways is largely attributed to a nonadrenergic, noncholinergic mechanism. While the specific transmitter(s) of this relaxant system have not been conclusively identified, vasoactive intestinal peptide and nitric oxide have emerged as likely mediators in airway smooth muscle. Both vasoactive intestinal peptide and nitric oxide relax guinea-pig, pig and human smooth muscle. Vasoactive intestinal peptide is present in nerve fibers associated with airway smooth muscle in humans and several animal species. In guinea-pigs, vasoactive intestinal peptide is released during electrical field stimulation of airway strips and the release correlates with the nonadrenergic relaxation. This relaxation is markedly reduced after incubation of tracheal tissue with a specific VIP antibody and by immunization to vasoactive intestinal peptide. Similarly, nonadrenergic relaxations induced by electrical field stimulation are reduced in human, pig, guinea-pig and bovine airways by nitric oxide synthesis inhibitors. Vasoactive intestinal peptide is present in nerve cell bodies of airway ganglia, suggesting that these nerves in airway smooth muscle originate from intrinsic neurons. It is stored in dense-core vesicles of nerve terminals near airway smooth muscle, suggesting that preformed vasoactive intestinal peptide is released by fusion of the vesicles with the cell membrane of the nerve terminal. Nitric oxide is probably generated by a novel mechanism involving de novo synthesis at the nerve terminal during neural activation by the action of the enzyme nitric oxide synthase.(ABSTRACT TRUNCATED AT 250 WORDS)
在人类、豚鼠、猫和猪的气道中，神经介导的平滑肌舒张在很大程度上归因于一种非肾上腺素能、非胆碱能机制。虽然该舒张系统的特定递质尚未得到最终确定，但血管活性肠肽和一氧化氮已成为气道平滑肌中可能的介质。血管活性肠肽和一氧化氮均可使豚鼠、猪和人类的平滑肌舒张。在人类和几种动物物种中，血管活性肠肽存在于与气道平滑肌相关的神经纤维中。在豚鼠中，气道条带受到电场刺激时会释放血管活性肠肽，且这种释放与非肾上腺素能舒张相关。用特异性VIP抗体孵育气管组织以及对血管活性肠肽进行免疫后，这种舒张作用会明显减弱。同样，一氧化氮合成抑制剂可使人类、猪、豚鼠和牛气道中由电场刺激诱导的非肾上腺素能舒张作用减弱。血管活性肠肽存在于气道神经节的神经细胞体中，这表明气道平滑肌中的这些神经起源于内在神经元。它储存于气道平滑肌附近神经末梢的致密核心囊泡中，这表明预先形成的血管活性肠肽是通过囊泡与神经末梢细胞膜融合而释放的。一氧化氮可能是通过一种新机制产生的，即在神经激活过程中，由一氧化氮合酶的作用在神经末梢进行从头合成。（摘要截选至250词）
