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Role of sensory neuropeptides in post‐allergic propranolol‐induced bronchoconstriction in guinea pigs in vivo
Author(s) -
FUJIMURA M.,
TSUJIURA M.,
MYOU S.,
ISHIURA Y.,
MATSUDA T.
Publication year - 1996
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.1996.tb00545.x
Subject(s) - bronchoconstriction , propranolol , substance p , guinea pig , medicine , neurokinin a , neuropeptide , antagonist , immunology , pharmacology , inhalation , endocrinology , anesthesia , asthma , receptor
Summary Background Administration of propranolol can provoke bronchoconstriction in asthmatic patients. We hypothesized that such bronchoconstriction may result from the inflammatory mediators released by an allergic reaction. We recently developed a guinea pig model for propranolol‐induced bronchoconstriction (PIB). Neuropeptides which are released from C‐fibre nerve endings have been postulated to induce bronchial hyperresponsiveness through neurogenic inflammation. Objective The purpose of this study was to examine whether sensory neuropeptides are involved in the development of PIB after allergic reaction. Methods Propranolol at a concentration of 10mg/ml was inhaled 20min after antigen challenge in passively sensitized, anaesthetized and artificially ventilated guinea pigs. The animals were treated intravenously with a NK 1 and NK 2 dual antagonist, FK224, in a dose of 1 or 10 mg/kg or vehicle or a selective NK 1 antagonist, FK888, in a dose of 1 or 10mg/kg or vehicle 10min before or 15min after antigen challenge. Results Propranolol inhaled 20 min after antigen challenge caused bronchoconstriction. FK224 or FK888 administered 15 min after antigen challenge as well as 10 min before antigen challenge did not reduce the PIB. Conclusion We conclude that neuropeptides such as neurokinin A and substance P do not directly contribute to the development of PIB after allergic reaction.