The human lung mast cell is a crucial effector cell in the mediation of asthma. Activation of mast cells by allergens, and other insults, leads to the elaboration of a wide variety of autacoids that cause bronchoconstriction and promote inflammation. Of the drugs that are used to treat asthma, only bronchodilator beta2-adrenoceptor agonists are effective at inhibiting the elaboration of mediators from mast cells. Both short- and long-acting beta2-adrenoceptor agonists are effective inhibitors of mast cells although there are differences in the degree of inhibitory activity attained with a given agonist. Human lung mast cells express a homogeneous population of beta2-adrenoceptors. However, the density of beta2-adrenoceptors differs from preparation to preparation and this may influence the extent to which agonists stabilise mast cell activity. Tolerance to the mast cell-stabilising activity of beta2-adrenoceptor agonists can be readily demonstrated. As a generalisation, agonists that are more effective inhibitors of mediator release also induce greater levels of tolerance although weaker agonists induce greater levels of tolerance than might be expected. However, the extent of tolerance does not correlate with the degree of beta2-adrenoceptor loss. The inhibitory activity of agonists and the extent of tolerance observed may be influenced by genetic polymorphisms in the gene for the beta2-adrenoceptor.