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Effects of β 2 ‐adrenoceptor agonists on anti‐IgE‐induced contraction and smooth muscle reactivity in human airways
Author(s) -
Gorenne Isabelle,
Labat Carlos,
Norel Xavier,
Montpreville Vincent,
Guillet MarieChristine,
Cavero Icilio,
Brink Charles
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb13294.x
Subject(s) - contraction (grammar) , muscle contraction , endocrinology , adrenergic receptor , medicine , immunoglobulin e , smooth muscle , receptor , chemistry , pharmacology , immunology , antibody
1 The β 2 ‐adrenoceptor agonists, salbutamol, salmeterol and RP 58802 relaxed basal tone of human isolated bronchial smooth muscle. Salmeterol‐ and RP 58802‐induced relaxations persisted for more than 4h when the medium was constantly renewed after treatment. 2 Salbutamol, salmeterol and RP 58802 reversed histamine‐induced contractions in human airways (pD 2 values: 6.15 ± 0.21, 6.00 ± 0.19 and 6.56 ± 0.12, respectively). 3 Anti‐IgE‐induced contractions were significantly inhibited immediately after pretreatment of preparations with β 2 ‐adrenoceptor agonists (10 μ m ). However, when tissues were treated with β 2 ‐agonists and then washed for a period of 4 h, salmeterol was the only agonist which significantly inhibited the anti‐IgE response. 4 Histamine response curves were shifted to the right immediately after pretreatment of tissues with the β 2 ‐adrenoceptor agonists (10 μ m ; 20 min), but maximal contractions were not affected. After a 4 h washing period, the histamine curves were not significantly different from controls. Concentration‐effect curves to acetylcholine (ACh) or leukotriene C 4 (LTC 4 ) were not significantly modified after β 2 ‐agonist pretreatment. 5 These results suggest that β 2 ‐adrenoceptor agonists may prevent anti‐IgE‐induced contraction by inhibition of mediator release rather than alterations of those mechanisms involved in airway smooth muscle contraction.