Noradrenergic inhibitory innervation of canine airways

The inhibitory innervation of canine airways was examined in isolated trachealis strips and helical strips of airways having outside diameters of 5 and 1.5 mm. Exogenous norepinephrine (10-8 M to 10-3 M) did not alter resting tone but relaxed airways contracted by 10-5 M histamine. Relaxations produced by norepinephrine were antagonized by 10-6 M propranolol, demonstrating the presence of beta-adrenergic receptors. Trans-ural electric stimulation also inhibited contractions produced by histamine. These electrically induced relaxations were blocked by tetrodotoxin and were reduced in magnitude by propranolol, indicating the involvement of a sympathetic neural mechanism. The inhibitory response to electric stimulation was attenuated in airways from catecholamine-depleted dogs and abolished in four of nine catecholamine-depleted airways pretreated with propranolol. Exogenous tyramine (10-5 M) also relaxed histamine-induced contractions, and this effect was blocked by propranolol or catecholamine depletion. The study showed that beta-adrenergic receptors from the trachea to 1.5-mm airways are innervated and that this sympathetic system constitutes the primary inhibitory innervation of airway smooth muscle in the dog.