Journal of Applied Physiology AJP: Cell Physiology
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J Appl Physiol 80: 1973-1977, 1996;
8750-7587/96 $5.00
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Journal of Applied Physiology, Vol 80, Issue 6 1973-1977, Copyright © 1996 by American Physiological Society

ARTICLES

Effect of thromboxane A2-receptor antagonist on bradykinin-induced bronchoconstriction in asthma

K. Rajakulasingam, S. L. Johnston, J. Ducey, W. Ritter, P. H. Howarth and S. T. Holgate
Department of Allergy and Immunology, National Heart and Lung Institute, London, United Kingdom.

The role of the thromboxane A2 (TxA2) receptor in bradykinin-induced bronchial responses was investigated in this study by using a selective and potent TxA2-receptor antagonist BAY u 3405. Eleven asthmatic subjects were randomized to receive 50 mg of BAY u 3405 or matched placebo in a crossover and double-blind fashion. Ninety minutes after dosing, serum was taken for drug assay, and subjects underwent provocation with bradykinin or prostaglandin D2 (PGD2) to determine bronchial responsiveness [provocative concentration of agonist required to produce a 20% fall in forced expiratory volume in 1 s from the postdiluent baseline (PC20)]. Pretreatment with BAY u 3405 caused a twofold doubling-dilution reduction in bronchial reactivity to PGD2; the geometric mean PC20 values were 0.132 (0.015-0.871) and 0.034 (0.008-0.095) mg/ml, respectively, for active and placebo days (P = 0.001). There was, however, no significant difference in PC20 values for bradykinin between active and placebo treatment days. We have demonstrated that BAY u 3405 caused a significant inhibition of bronchconstriction induced by inhaled PGD2 but had no influence on bronchial responsiveness to inhaled bradykinin. This study suggests therefore that TxA2 receptors do not play a role in bradykinin-induced bronchoconstriction in asthma.


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