Sensory neuropeptides are not involved in acetaldehyde-induced bronchoconstriction in guinea-pigs

1. Alcohol-induced asthma is characterized by worsening of asthmatic symptoms after alcohol ingestion. Acetaldehyde, a metabolite of ethanol, is thought to be a main factor of alcohol-induced asthma. Although airway sensory nerves are known to be activated in asthma, there have been no studies investigating the role of tachykinins in the airway response to acetaldehyde. The purpose of the present study was to evaluate the involvement of tachykinins on acetaldehyde-induced bronchoconstriction in guinea-pigs. 2. After capsaicin desensitization or intravenous administration of 10 mg kg(-1) FK224, a NK1 and NK2 dual antagonist, airway responses to ascending doses (2.5-20 mg ml(-1)) of inhaled acetaldehyde was examined using a modified Konzett-Rössler method in guinea-pigs. 3. Inhalation of acetaldehyde induced bronchoconstriction in a dose-dependent manner. The FK224 failed to reduce the acetaldehyde-induced bronchoconstriction. Pretreatment with capsaicin did not alter the bronchoconstriction induced by acetaldehyde at a dose of 2.5-10 mg ml(-1). Pretreatment with capsaicin slightly, but significantly, inhibited bronchoconstriction induced by 20 mg ml(-1) of acetaldehyde. 4. The present results suggest that tachykinins are not involved in acetaldehyde-induced bronchoconstriction in guinea-pigs.