Pieces of ferret trachea and human bronchi were mounted in Ussing chambers and given [35S]sulphate as a radiolabelled precursor of mucous glycoproteins (mucins). The output of 35S bound to macromolecules was studied as an index of mucin secretion. In the ferret trachea, electrical field stimulation increased the rate of mucin secretion. Tetrodotoxin (10(-7) M or 10(-6) M) abolished this effect. Pilocarpine (25 microM) stimulated the output of mucins from human bronchus. Atropine (10(-5) M) abolished this effect. Electrical field stimulation of human bronchus stimulated mucin secretion. Tetrodotoxin (10(-6) M) abolished this effect. Field stimulation in the presence of either atropine (10(-5) M) or atropine with l-propranolol (10(-5) M) and phentolamine (10(-5) M) caused no stimulation of mucin secretion rate. Some bronchi were treated with noradrenaline (10(-5) M) for 1 h to allow the adrenergic nerves to take up transmitter. Even in these, atropine prevented the effect of field stimulation. We conclude that activity in cholinergic nerves can stimulate mucin secretion in the bronchi in man. Our results provide no evidence that the adrenergic nerves or non-adrenergic, non-cholinergic nerves have a direct action on bronchial secretory cells in man.