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首页> 外文期刊>Pulmonary pharmacology & therapeutics >Nerve growth factor enhances neurokinin A-induced airway responses and exhaled nitric oxide via a histamine-dependent mechanism.
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Nerve growth factor enhances neurokinin A-induced airway responses and exhaled nitric oxide via a histamine-dependent mechanism.

机译：神经生长因子通过组胺依赖性机制增强神经激肽A诱导的气道反应和呼出的一氧化氮。

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The neurotrophin nerve growth factor (NGF) is elevated in serum and locally in the lung in asthmatics and has been suggested to evoke airway hyperresponsiveness. The aim of this study was to explore mechanisms behind NGF-evoked changes in airway responsiveness. We studied if NGF could evoke increased airway responsiveness to tachykinins, such as neurokinin A (NKA), in a similar way as for histamine and, if so, whether an NGF-evoked increase in NKA airway responsiveness could involve a histamine receptor-dependent mechanism. Contractile responses to cumulative doses of histamine or NKA were studied in guinea-pig tracheal rings in vitro in organ baths. Furthermore, insufflation pressure (IP), pulmonary resistance, lung compliance and exhaled NO (FeNO) were measured in vivo in anaesthetised guinea-pigs challenged with histamine or NKA. NGF pre-treatment in vitro increased the contractile response evoked by histamine, but not by NKA, in tracheal rings. NGF pre-treatment in vivo increased IP, pulmonary resistance and levels of FeNO, and further decreased lung compliance, upon histamine and NKA challenge. The NGF-evoked enhancement of IP, pulmonary resistance, lung compliance as well as FeNO in response to NKA was reversed by the histamine receptor antagonist mepyramine. We suggest that NGF can induce an increase in tachykinin-evoked airway responses and NO formation via a histamine receptor-dependent pathway. This points to an important role for the mast cell in neurotrophin-evoked airway hyperresponsiveness and changes in exhaled NO.
机译：哮喘患者的神经营养蛋白神经生长因子（NGF）在血清中和肺中局部升高，并被认为可引起气道高反应性。这项研究的目的是探讨NGF引起气道反应性改变的机制。我们研究了NGF是否可以以与组胺相似的方式引起对速激肽如神经激肽A（NKA）的气道反应性的增强，如果是，那么NGF引起的NKA气道反应性的增强是否可能涉及组胺受体依赖性机制。在器官浴中，在豚鼠气管环中研究了对累积剂量的组胺或NKA的收缩反应。此外，在体内用组胺或NKA刺激的豚鼠体内测量了吹入压力（IP），肺阻力，肺顺应性和呼出NO（FeNO）。 NGF的体外预处理可增强气管环中由组胺引起的收缩反应，但不能由NKA引起。在组胺和NKA刺激下，体内NGF预处理可提高IP，肺抵抗力和FeNO含量，并进一步降低肺顺应性。 NGF引起的IP，肺阻力，肺顺应性以及FeNO对NKA的增强作用被组胺受体拮抗剂美吡拉明逆转。我们建议NGF可以通过组胺受体依赖性途径诱导速激肽诱发的气道反应和NO形成增加。这表明肥大细胞在神经营养蛋白引起的气道高反应性和呼出NO的变化中起重要作用。

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