Involvement of α_2-Adrenergic Receptors in the Vagal Reflex-Induced Tracheal Constriction

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The effects of clonidine on the vagal reflex-induced tracheal constriction have been investigated in anesthetized, paralyzed, and artificially ventilated mongrel dogs. The cervical trachea was transected in situ into two parts. Responses of the tracheal musculature were measured as changes in the intratracheal pressure on an air-filled balloon introduced into the rostral side of the transected trachea. Reflex tracheal constriction was induced by afferent electrical stimulation at the central cut end of the vagus nerve. Drugs were injected or infused close intraarterially (i.a.) into the bilateral cranial thyroid arteries in such a way that each drug was applied just to the rostral trachea. The reflex tracheal constriction was abolished by a close i.a. infusion of 3 μM atropine. The magnitude of the reflex tracheal constriction was slightly reduced by a close i.a. infusion of 10μM clonidine and was significantly reduced by the infusion of clonidine at a concentration of 100 and 300μM. The response to 100μM clonidine was antagonized by a close i.a. infusion of 1μM yohimbine. The tracheal constriction induced by i.a. injection of 5.5 nmol acetylcholine was unaffected by infusion of 10,100 and 300μM clonidine. The vagal reflex-induced tracheal constriction seems to be inhibited by stimulation of prejunctional α_2-adrenoceptors.
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