Ethanol-induced bronchodilatation in TEA-treated canine tracheal smooth muscle is mediated by a beta-adrenoceptor-dependent mechanism.

The effects of moderate concentrations of ethanol (8-34 mM) on the electromechanical activity of airway smooth muscle cells of canine trachealis, stimulated by the spasmogen tetraethylammonium (TEA), are described for in vitro and cultured reaggregate preparations. Ethanol produced a concentration-dependent hyperpolarization, and suppression of action potentials in smooth muscle preparations, in vitro, whereas it was without effect in cultured airway smooth muscle cells. In the presence of the beta-adrenoceptor antagonist propranolol (1 microM), ethanol had no effect on in vitro preparations. Isoproterenol (0.1 microM) produced hyperpolarization and suppression of action potentials in airway smooth muscle of both preparations. These effects were not observed when propranolol was additionally present. This suggests that both in vitro, and cultured airway smooth muscle preparations maintained their beta-receptors, and that ethanol caused the release of endogenous catecholamine from adrenergic nerve endings which apparently remained intact in in vitro, but not in cultured airway smooth muscle preparations.