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Relationships between Responsiveness of the Bronchi to Acetylcholine and Cyclic AMP Response of Lymphocytes to Beta 1 ‐ and Beta2‐Adrenergic Receptor Stimulation in Patients with Asthma
Author(s) -
Makino Sohei,
Ikemori Ryosuke,
Fukuda Takiishi,
Motojima Shinji
Publication year - 1983
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.1983.tb00854.x
Subject(s) - asthma , salbutamol , beta (programming language) , medicine , endocrinology , acetylcholine , stimulant , stimulation , adrenergic receptor , adrenergic , beta 1 adrenergic receptor , receptor , computer science , programming language
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, 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 cyclic AMP 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 FEV 1 of more than 20% of the baseline value. Beta 1 and heta 2 ‐responses were expressed as the increments of cyclic AMP content of 10 6 lymphocytes incubated with norepinephrine (beta 1 ‐stimulant) and salbutamol (beta 2 ‐stimulant). RT‐Ach showed a significant correlation with the beta 2 ‐cyclic AMP 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. These results suggest that selective beta 2 ‐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 administration of beta‐stimulants is discussed.