Histamine-evoked acetylcholine release in sensitized tracheal preparation

The contractile response to histamine of tracheal muscle was studied in preparations from BSA-sensitized and non-sensitized guinea-pigs. Sensitization,did not enhance the overall response to histamine. However, this response showed evidence of acetylcholine participation. In sensitized preparations, atropine (0.1 μM) caused a significant depression of the dose response to histamine (n = 11, p = 0.028), especially in tile range 2-8 μM. Physostigmine (0.1 μM) significantly potentiated the effect of histamine (n = 8, p = 0.003), especially at greater than 4 μM histamine. The response to histamine of non-sensitized preparations was not altered by atropine (n = 11) or physostigmine (n = 8). The following agents did not discriminate between sensitized and non-sensitized preparations: Famotidine, an H₂ antagonist; dimaprit, an H₂ agonist; thioperamide, an H₃ antagonist; α-methylhistamine; an H₃ agonist; gallamine, an M₂ antagonist, suggesting that muscarinic M, receptor dysfunction alone is not sufficient to cause bronchial hyper-responsiveness. The results show that sensitization causes a change ill the components of the contractile response to histamine rather than bronchial hyper-responsiveness to this agent.