1. We describe a method for supporting pieces of human bronchi in Ussing chambers, for radiolabelling the contents of the secretory cells with 35S, and for collecting radiolabeled macromolecules secreted on to the luminal aspect of the tissue. This method has previously been used to study airway secretions in animals [R. J. Phipps, J. A. Nadel & B. Davis, American Review of Respiratory Disease, (1980) 121, 359–365]. Evidence is given that the radiolabelled molecules are secretory glycoproteins, probably mucus glycoproteins.
2. Phenylephrine, an α-adrenoceptor agonist, increased the rate at which the bronchi secreted radiolabeled glycoproteins. Thymoxamine, an α-adrenoceptor antagonist, blocked this effect but propranolol, a β-adrenoceptor antagonist, did not.
3. Dobutamine, a β1-adrenoceptor agonist, increased the rate of secretion of radiolabeled glycoproteins. Propranolol blocked this but thymoxamine did not.
4. Salbutamol, a β2-adrenoceptor agonist, also increased the rate of secretion of radiolabeled glycoproteins. Propranolol blocked this effect.
5. We conclude that both α and β-adrenoceptor agonists increase the rate of glycoprotein secretion in human bronchi in vitro and that this almost certainly means that they increase the rate of mucus secretion.