The aims of the present studies were to investigate sympatho-adrenal mechanisms and adrenergic receptor function in patients with bronchial asthma and healthy subjects. The patients were characterized with regard to the occurrence of exercise-, histamine- or allergen-induced bronchoconstriction in pre-trial tests. All medication was withdrawn during at least one week prior to the trials, in order to eliminate the influence of treatment. The patients were asymptomatic and had basal PEFR greater than 70% of predicted values prior to the trials. Healthy control subjects were matched with regard to sex and age. Alpha- and beta-adrenoceptor responsiveness were studied with improved in vivo-techniques, where different responses were related to plasma concentrations rather than doses of the agonists administered. Sympatho-adrenal reactivity, as assessed by plasma noradrenaline and adrenaline responses, to an orthostatic test and exercise was normal in asthmatic subjects. Surprisingly, there was no plasma catecholamines response to histamine- or allergen-induced bronchoconstriction. High plasma levels of noradrenaline and phenylephrine (by i.v. infusion) had little or no influence on bronchial tone, despite marked cardiovascular effects, in patients with exercise-induced asthma (EIA) or healthy subjects. Elevation of circulating noradrenaline failed to alter bronchial hyperreactivity to histamine in asthmatic patients. The blood pressure responses to infused noradrenaline and phenylephrine were similar in patients with EIA and healthy subjects, but the ensuing bradycardia was more pronounced in the EIA-patients indicating an increased baroreceptor sensitivity in these patients. High, but physiological, plasma levels of adrenaline dilated the airways with regard to end-expiratory flow rates but not Sgaw or PEFR. Furthermore, allergen-induced bronchoconstriction was counteracted by elevation of circulating adrenaline in patients with allergic asthma. These findings indicate that adrenaline may participate in the regulation of airway tone under physiological conditions. Beta 2-adrenoceptor sensitivity was found to be reduced in patients with EIA when assessed by both in vitro and in vivo techniques, while patients with non-exercise induced asthma did not differ from controls in this respect. Lymphocytes from EIA-patients had a reduced cAMP response to isoprenaline. Furthermore, the beta 2-mediated increase in plasma cAMP and the reduction of diastolic blood pressure in response to i.v. isoprenaline infusions were attenuated in the EIA-patients. These results do not seem to be influenced by previous anti-asthmatic drug treatment or the severity of the disease.(ABSTRACT TRUNCATED AT 400 WORDS)