RT Journal Article SR Electronic T1 Tachykinins and airway microvascular leakage induced by HCl intra-oesophageal instillation JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP 268 OP 273 DO 10.1183/09031936.02.00250902 VO 20 IS 2 A1 S. Daoui A1 B. D'Agostino A1 L. Gallelli A1 X. Emonds Alt A1 F. Rossi A1 C. Advenier YR 2002 UL http://erj.ersjournals.com/content/20/2/268.abstract AB Gastro-oesophageal reflux is a common clinical disorder associated with a variety of respiratory symptoms, including chronic cough and exacerbation of asthma. In this study, the potential role of acid-induced tachykinin release was examined in guinea pigs and rabbits, by examining the effects of the tachykinin NK1 and NK3 receptors antagonists (SR 140333 and SR 142801, respectively) (1–10 mg·kg−1) on plasma protein extravasation induced in airways by hydrochloric acid (HCl) infusion in the oesophagus. Guinea pigs were anaesthetised with urethane, while rabbits were subject to neuroleptoanalgesia with hypnorm. Airway vascular leakage was evaluated by measuring extravasation of Evans blue dye. All animals were pretreated with atropine (1 mg·kg−1 i.p.), propranolol (1 mg·kg−1 i.p.), phosphoramidon (2.5 mg·kg−1 i.v.) and saline or tachykinin receptor antagonists (1–10 mg·kg−1 i.p.). Infusion of 1 N HCl into the oesophagus led to a three- and five-fold increase in plasma extravasation in the main bronchi and trachea, respectively. This increase was largely prevented by the tachykinin NK1 and NK3 receptor antagonists SR 140333 and SR 142801 (1–10 mg·kg−1). These results suggest that protein extravasation in the airways, as induced by intra-oesophageal HCl infusion, is mainly dependent on the release of tachykinins, and that both NK1 and NK3 tachykinin receptors are involved. The results suggest that HCl-induced sensory nerve stimulation may act in the periphery on intermediate neurons and/or ganglia where NK3 receptors have been shown to play an important role.