Tachykinins activate guinea‐pig alveolar macrophages: involvement of NK2 and NK1 receptors

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Abstract
1 The effects of substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) were evaluated on superoxide anion () production by guinea-pig alveolar macrophages (AM). 2 SP dose-dependently (ED50 = 0.7 nm) evoked production from guinea-pig AM; the N-terminal heptapeptide, SP(1–7), was ineffective. In the presence of thiorphan (10−5 m), an enkephalinase inhibitor, the stimulating effects of SP were not significantly modified. NKA and NKB were both able to induce production from guinea-pig AM, ED50 values being 0.1 and 1.3 nm, respectively. Therefore, the rank order of activity of natural tachykinins was NKA > SP > NKB. Tachykinin-evoked effects were quantitatively similar to those elicited by the autacoid mediator PAF-acether and less than those induced by the synthetic peptide N-formylmethionyl-leucyl-phenylalanine (FMLP). 3 The NK2 receptor agonist [β-Ala8]-NKA (4–10) dose-dependently evoked production from guinea-pig AM; the NK1 receptor agonist [Pro9]-SP sulphone acted only at high concentrations, while the NK3 receptor agonist [Me, Phe7]-NKB was ineffective. 4 These findings indicate that guinea-pig AM possess NK2 and possibly some NK1 tachykinin receptors and further suggest tachykinin involvement in lung pathophysiology.

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