Autonomic responses of the isolated, innervated trachea of the guinea-pig: interaction with autonomic drugs, histamine and 5-hydroxytryptamine.

Intraluminal pressure was measured in the isolated, fluid-filled trachea of the guinea pig, with autonomic innervation on the right side intact. Increases or decreases in intraluminal pressure reflected excitatory or inhibitory responses respectively, in the tracheal smooth muscle. Stimulation of the cervical vagus nerve evoked a cholinergic excitatory response. After cholinergic blockade with atropine, a non-adrenergic, non-cholinergic inhibitory response was obtained. Stimulation of the cervical sympathetic trunk, or stellate ganglion, evoked beta-adrenergic inhibitory responses. In the presence of propranolol, sympathetic stimulation evoked alpha-adrenergic excitatory responses which were of low amplitude (less than or equal to 5% of cholinergic excitatory responses). In the presence of phentolamine but not prazosin, beta-adrenergic inhibitory responses were potentiated. Neostigmine potentiated responses to vagal stimulation, increasing the amplitude and duration of response. At higher concentrations neostigmine (i) raised intraluminal pressure, a response blocked by atropine, and (ii) attenuated sympathetic inhibitory responses, an effect largely blocked by atropine. Histamine increased intraluminal pressure and this response was attenuated by atropine. In the presence of histamine, vagal excitatory responses were attenuated. Sympathetic inhibitory responses at low frequencies of stimulation (up to 10 Hz) were inhibited by histamine. 5-Hydroxytryptamine (5-HT) increased intraluminal pressure also, an effect partially blocked by atropine. 5-HT had no effect on vagal excitatory responses. Like histamine, 5-HT attenuated sympathetic inhibitory responses at lower frequencies of stimulation.