Inhibition of the cholinergic neurotransmission in human airways via prejunctional alpha-2-adrenoceptors.

Previous investigations on guinea-pig airways indicate that the excitatory, cholinergic neurotransmission can be inhibited via prejunctional alpha-2-adrenoceptors. The aim of this study was to investigate whether a similar inhibition of the cholinergic neurotransmission is present in human airways. Ring preparations of human bronchi were mounted for recording of isometric tension and immersed in oxygenated Krebs solution. Electrical field stimulation of the preparations elicited atropine-sensitive twitch contractions. Exogenous noradrenaline (in the presence of cocaine and propranolol) inhibited the electrically evoked contractions. The noradrenaline-induced inhibition could be antagonized by yohimbine whereas prazosin was ineffective, indicating that the inhibition was mediated by alpha-2-adrenoceptors. Contractions evoked by exogenous acetylcholine (in the presence of cocaine and propranolol) was unaffected by the addition of noradrenaline, which suggests that the alpha-2-adrenoceptors have a prejunctional localization. In conclusion, this report gives evidence that the human bronchial, cholinergic neurotransmission can be inhibited by stimulation of prejunctional alpha-2-adrenoceptors.