Inhibitory effects of catecholamine in isolated canine bronchial smooth muscle

Abstract

Experiments were designed to investigate whether catecholamines affect cholinergic neurotransmission in the bronchial wall. Rings of canine bronchi were mounted for continuous isometric tension recording. Acetylcholine and electrical stimulation caused contractions. As the response to electrical stimulation was unaffected by hexamethonium, but inhibited by tetrodotoxin and atropine, it must be due to release of endogenous acetylcholine from postganglionic cholinergic nerves. Norepinephrine and isoproterenol inhibited the response to electrical stimulation significantly more than that to acetylcholine; propranolol abolished the inhibition in both cases. In the canine bronchi catecholamines possibly induce dilation during bronchoconstriction caused by increased cholinergic nerve activity, whereas they have relatively weak inhibitory effects on bronchial smooth muscle made to contract with exogenous acetylcholine. Propranolol augmented the contractile response to electrical stimulation, but not that to acetylcholine. Helical bronchial strips were incubated with [3H]norepinephrine and mounted for superfusion; the overflow of tritiated compounds in the superfusate was measured. Electrical stimulation augmented markedly the 3H efflux. The electric impulses apparently activate cholinergic and adrenergic nerves in the bronchial wall, and endogenously released norepinephrine can partially inhibit bronchoconstrictions caused by stimulation of the cholinergic nerves.