反对血管活性肠肽（VIP）作为气道神经源性反应中的扩张剂以及支持P物质作为收缩剂的证据。
Evidence against vasoactive intestinal polypeptide (VIP) as a dilator and in favour of substance P as a constrictor in airway neurogenic responses.
作者信息
Karlsson J A, Persson C G
出版信息
Br J Pharmacol. 1983 Jul;79(3):634-6. doi: 10.1111/j.1476-5381.1983.tb09999.x.
Abstract
Propranolol-resistant neurogenic relaxation persisted in (carbachol-contracted) guinea-pig tracheae already relaxed by supramaximal concentrations of vasoactive intestinal polypeptide (VIP). Also, VIP relaxed preparations that were under neurogenic inhibition. In hilus bronchi, about 60% of a neurogenic contraction was atropine-resistant. (Arg5, D-Trp7.9) SP 5-11 specifically antagonized this contraction and those produced by exogenous substance P. Substance P, but not VIP, seems to be involved in nerve-mediated effects on guinea-pig airway tone.
摘要
在已被超最大浓度的血管活性肠肽（VIP）松弛的（卡巴胆碱收缩的）豚鼠气管中，普萘洛尔耐药性神经源性松弛持续存在。此外，VIP使处于神经源性抑制状态的标本松弛。在肺门支气管中，约60%的神经源性收缩对阿托品耐药。（Arg5，D-Trp7.9）SP 5-11特异性拮抗这种收缩以及由外源性P物质产生的收缩。P物质而非VIP似乎参与了对豚鼠气道张力的神经介导作用。
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