In severe asthma attacks, beta 2-sympathomimetics can lose part of their therapeutic potency possibly due to a predominance of contractile mediators. To elucidate this loss of potency, we chose tracheal smooth muscle strips as experimental model which were partially and maximally precontracted with 100 and 6,000 nmol/l carbachol, respectively, reflecting different contractile states of the smooth muscle strips. Both contractures were dose-dependently relaxed by fenoterol and salbutamol which are well established as beta 2-sympathomimetics, by a new compound (formoterol) and by isoprenaline as standard. In tracheal strips, partially precontracted with 100 nmol/l carbachol, all agonists induced maximum relaxation beyond basal tone thereby characterized as full agonists. In maximally precontracted tracheal strips beta-adrenergic relaxation was markedly attenuated for all agonists by 70-80%. Maximum relaxation by the beta 2-sympathomimetics was even smaller than that of isoprenaline. By these experiments, the beta 2-sympathomimetics were characterized as partial agonists. The intrinsic 'activities (IA) for relaxation were different for the 3 beta 2-sympathomimetics investigated. Intrinsic activities were 0.8, 0.6 and 0.6 for formoterol, fenoterol and salbutamol, respectively. In both group of experiments formoterol exhibited the lowest EC50 for relaxation, which was 20 and 50 times lower than that of fenoterol and salbutamol, respectively. To investigate, if the higher relaxant potency of formoterol correlated to a higher binding affinity for beta 2-adrenoceptors, we performed radioligand binding experiments in guinea pig lung membranes. The non-linear regression analysis of data revealed a high affinity of formoterol, which was 16- and 40-fold higher than that of fenoterol and salbutamol, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)