Prejunctional beta 1-adrenoceptors inhibit cholinergic transmission in canine bronchi

• Published in: Journal of applied physiology (1985) Vol. 62; no. 2; p. 785
• Main Authors: Danser, A H, van den Ende, R, Lorenz, R R, Flavahan, N A, Vanhoutte, P M
• Format: Journal Article
• Language: English
• Published: United States 01.02.1987
• Subjects: Animals; Bronchi - innervation; Dogs; Female; In Vitro Techniques; Male; Neural Inhibition; Neuromuscular Junction - physiology; Parasympathetic Nervous System - physiology; Perfusion; Receptors, Adrenergic, beta - physiology; Sympathomimetics - pharmacology; Synaptic Transmission
• ISSN: 8750-7587
• DOI: 10.1152/jappl.1987.62.2.785

The aim of the present study was to determine in canine bronchi the effects produced by norepinephrine (released from adrenergic nerve terminals) on cholinergic neurotransmission. Electrical stimulation of canine bronchi activates cholinergic and adrenergic nerve fibers. The adrenergic neuronal blocker, bretylium tosylate, inhibited the increase in [3H]norepinephrine overflow evoked by electrical stimulation but did not prevent that caused by the indirect sympathomimetic tyramine. During blockade of the exocytotic release of norepinephrine with bretylium, the pharmacological displacement of the sympathetic neurotransmitter by tyramine significantly decreased the contractions evoked by electrical stimulation but did not affect contractions caused by exogenous acetylcholine. Metoprolol, a beta 1-adrenergic antagonist, abolished and propranolol significantly reduced the effect of tyramine during electrical stimulation. alpha 2-Adrenergic blockade, beta 2-adrenergic blockade, or removal of the epithelium did not significantly affect the response to tyramine. These results suggest that norepinephrine when released from sympathetic nerve endings can activate prejunctional inhibitory beta 1-adrenoceptors to depress cholinergic neurotransmission in the bronchial wall.