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 microM) caused a significant depression of the dose response to histamine (n = 11, p = 0.028), especially in the range 2-8 microM. Physostigmine (0.1 microM) significantly potentiated the effect of histamine (n = 8, p = 0.003), especially at greater than 4 microM 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; alpha-methylhistamine, an H3 agonist; gallamine, an M2 antagonist, suggesting that muscarinic M2 receptor dysfunction alone is not sufficient to cause bronchial hyper-responsiveness. The results show that sensitization causes a change in the components of the contractile response to histamine rather than bronchial hyper-responsiveness to this agent.