Decreased response of beta‐adrenergic receptor has been considered to he one of the causes of increased responsiveness of the bronchi in asthma. Since beta‐adrenergic receptor has two subtypes, beta1and beta2, and the bronchodilating effect of beta stimulants is mediated by beta2‐receptor, responsiveness of the bronchi is expected to correlate to the cyclic AMP response of lymphocytes to a beta2‐stimulant. Responsiveness of the bronchi was expressed as respiratory threshold to acetylcholine (RT‐Ach), which was the minimal concentration of acetylcholine solution to cause an initial decrease of FEV1of more than 20% of the baseline value. Beta1and heta2‐responses were expressed as the increments of cyclic AMP content of 106lymphocytes incubated with norepinephrine (beta1‐stimulant) and salbutamol (beta2‐stimulant).RT‐Ach showed a significant correlation with the beta2‐cyclic AMP response of lymphocytes, but not with the beta1‐response among patients with asthma. Sixteen symptomatic patients on continuous beta‐stimulants showed lower RT‐Ach value and diminished beta2‐receptor activity of lymphocytes compared with 14 patients in remission. These results suggest that selective beta2‐adrenergic blockade may he one of the causes of bronchial hypersensitivity in asthma, though it should be noted that in this study beta‐adrenergic responses were examined in lymphocytes and were compared with the responsiveneness of the bronchi. Possible beta‐receptor subsensitivity induced by administratio