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Tachykinin NK2 receptor antagonists decrease eicosanoid release in lung anaphylaxis

P Montuschi1, D Currò, G Ciabattoni

  • 1Department of Pharmacology, Faculty of Medicine, Catholic University of the Sacred Heart, Roma, Italy.

European Journal of Pharmacology
|October 10, 1996
PubMed
Summary
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Tachykinins contribute to anaphylaxis by increasing arachidonic acid metabolites. NK2 receptor antagonists reduced bronchoconstriction and eicosanoid release in guinea-pig lungs during allergic reactions.

Area of Science:

  • Pharmacology
  • Immunology
  • Respiratory Medicine

Background:

  • Tachykinins are implicated in inflammatory responses.
  • The role of tachykinins in lung anaphylaxis requires further investigation.

Purpose of the Study:

  • To investigate the role of tachykinins in guinea-pig lung anaphylaxis.
  • To assess the effects of tachykinin NK2 receptor antagonists on anaphylactic responses.

Main Methods:

  • In vitro perfused sensitized guinea-pig lungs.
  • Antigen challenge to induce anaphylaxis.
  • Administration of tachykinin NK2 receptor antagonists (MEN 10.627 and MEN 10.376).
  • Measurement of bronchoconstriction, thromboxane, and prostaglandin E2 release.

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Main Results:

  • Both NK2 receptor antagonists dose-dependently reduced antigen-induced bronchoconstriction.
  • Antagonists significantly decreased the release of thromboxane and prostaglandin E2.
  • No effect was observed on the basal release of eicosanoids.

Conclusions:

  • Tachykinins released from sensory nerves contribute to anaphylactic reactions.
  • Tachykinins mediate increased arachidonic acid metabolite release during anaphylaxis.
  • NK2 receptor antagonists show potential in managing allergic airway inflammation.