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Relationships between responsiveness of the bronchi to acetyl choline and cyclic amp response of lymphocytes to beta 1 adrenergic receptor and beta 2 adrenergic receptor stimulation in patients with asthma



Relationships between responsiveness of the bronchi to acetyl choline and cyclic amp response of lymphocytes to beta 1 adrenergic receptor and beta 2 adrenergic receptor stimulation in patients with asthma



Allergy 38(1): 37-42



Decreased response of .beta.-adrenergic receptor is considered one of the causes of increased responsivness of the bronchi in asthma. Since .beta.-adrenergic receptor has 2 subtypes, .beta.1 and .beta.2, and the bronchodilating effect of .beta. stimulants is mediated by .beta.2-receptor, responsiveness of the bronchi is expected to correlate to the cAMP response of lymphocytes to a .beta.2-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 FEV1 [1-s forced expiratory volume] of > 20% of the baseline value. .beta.1- and .beta.2-responses were expressed as the increments of cAMP content of 106 lymphocytes incubated with norepinephrine (.beta.1-stimulant) and salbutamol (.beta.2-stimulant). RT-Ach showed a significant correlation with the .beta.2-cAMP response of lymphocytes, but not with the .beta.1-response among patients with asthma. Sixteen symptomatic patients on continuous .beta.-stimulants showed lower RT-Ach value and diminished .beta.2-receptor activity of lymphocytes compared with 14 patients in remission. Selective .beta.2-adrenergic blockade may be one of the causes of bronchial hypersensitivity in asthma, though it should be noted than .beta.-adrenergic responses were examined in lymphocytes and were compared with the responsiveness of the bronchi. Possible .beta.-receptor subsensitivity induced by administration of .beta.-stimulants is discussed.

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