Lindberg S, Dolata J, Mercke U
Regul Pept. 1986 Dec 1;16(1):15-25. doi: 10.1016/0167-0115(86)90191-6.
Substance P (SP) released from sensory C-fibers in the airways increases the mucociliary (m.c.) activity in the rabbit maxillary sinus. The purpose of the present study was to investigate the m.c. effects of two other neuropeptides, coexisting with SP in sensory neurones, neurokinin A (NKA) and calcitonin gene-related peptide (CGRP). NKA increased the m.c. activity dose-dependently (dose range 0.1-10.0 micrograms/kg, 88 pmol to 8.8 nmol/kg), the maximum increase being 41.9 +/- 2.6%. The effect was inhibited by pretreatment with the tachykinin antagonist (D-Pro2,D-Trp7,9)SP, but not with atropine or hexamethonium. Thus NKA released from sensory C-fibers may contribute to the non-cholinergic increase of m.c. activity observed after C-fiber stimulation. In contrast CGRP did not influence the m.c. activity. Neither did it influence the responses to NKA or SP. It is concluded that CGRP is unlikely to be involved in the control of m.c. function.
气道中感觉性C纤维释放的P物质（SP）可增强兔上颌窦的黏液纤毛（m.c.）活性。本研究的目的是探究另外两种与SP共存于感觉神经元中的神经肽——神经激肽A（NKA）和降钙素基因相关肽（CGRP）的m.c.效应。NKA剂量依赖性地增强m.c.活性（剂量范围为0.1 - 10.0微克/千克，88皮摩尔至8.8纳摩尔/千克），最大增幅为41.9±2.6%。速激肽拮抗剂（D - Pro2，D - Trp7,9）SP预处理可抑制该效应，但阿托品或六甲铵预处理则无此作用。因此，感觉性C纤维释放的NKA可能促成了C纤维刺激后所观察到的m.c.活性的非胆碱能性增强。相比之下，CGRP并不影响m.c.活性，也不影响对NKA或SP的反应。结论是，CGRP不太可能参与m.c.功能的调控。
