Mercke U, Lindberg S, Dolata J
Rhinology. 1987 Jun;25(2):89-93.
Substance P (SP) released from sensory C-fibres 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 0.1-5.0 micrograms/kg) the maximum increase being 33.6 +/- 6.0%. 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-fibres may contribute to the non-cholinergic increase of m.c. activity observed after C-fibre 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。本研究的目的是研究另外两种与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）对黏液纤毛的作用。NKA剂量依赖性地增强黏液纤毛活性（剂量范围为0.1 - 5.0微克/千克），最大增幅为33.6±6.0%。速激肽拮抗剂（D - Pro2，D - Trp7,9）SP预处理可抑制该作用，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纤维刺激后观察到的黏液纤毛活性的非胆碱能性增强。相比之下，CGRP不影响黏液纤毛活性。它也不影响对NKA或SP的反应。结论是，CGRP不太可能参与黏液纤毛功能的调控。
