Parasympathetic ganglia in the airways.
Catecholamines seem to inhibit transmission through airway parasympathetic ganglia by two mechanisms: Beta-2-adrenoceptor stimulation induces a ganglionic inhibition characterised by: slow onset, effect mainly on neural signals of high frequency, localisation to the presynaptic nerve terminal in the ganglion (inhibition of transmittor release). In vivo this mechanism could be operated upon by circulating adrenaline, which is active on beta-2-adrenoceptors. Alpha-adrenoceptor stimulation induces a ganglionic inhibition characterised by: rapid onset, localisation to the presynaptic level (inhibition of transmittor release). This mechanism could be operated upon by noradrenaline released by sympathetic nerves supplying airway ganglia. In bronchial hyperreactivity the effect of catecholamines on transmission through airway ganglia could serve as a negative feed back mechanism reducing bronchoconstriction induced by neural reflexes. Tentatively, fascilitation of transmission through airway ganglia could contribute to bronchial hyperreactivity. However, such fascilitation has not yet been demonstrated for airway ganglia, although it has been found in sympathetic ganglia.
D000818:Animals; D004558:Electric Stimulation; D005289:Ferrets; D005726:Ganglia, Parasympathetic / Q000502:physiology*; D009433:Neural Inhibition; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D013268:Stimulation, Chemical; D009435:Synaptic Transmission / Q000187:drug effects; D014132:Trachea / Q000294:innervation*
D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta