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Bradykinin‐induced bronchoconstriction: inhibition by nedocromil sodium and sodium cromoglycate.
Author(s) -
Dixon CM,
Barnes PJ
Publication year - 1989
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1989.tb03446.x
Subject(s) - nedocromil sodium , bronchoconstriction , nedocromil , bradykinin , cromolyn sodium , placebo , inhalation , asthma , anesthesia , medicine , pharmacology , chemistry , alternative medicine , receptor , pathology
1. The effects of inhaled nedocromil sodium and sodium cromoglycate on bradykinin‐induced bronchoconstriction have been studied in a double‐ blind, placebo controlled study, in eight mild asthmatic subjects. 2. The subjects attended on four occasions. Fifteen minutes after drug pre‐ treatment a bradykinin challenge was performed. Increasing concentrations were inhaled until a greater than 40% fall in expiratory flow at 30% of vital capacity from a partial flow volume manoeuvre (V p30) was demonstrated. 3. Inhaled bradykinin (0.06‐8.0 mg ml‐1) caused dose‐related bronchoconstriction with the geometric mean cumulative dose causing a 40% fall in V p30 (PD40) of 0.035 (95% CI: 0.02‐0.07) mumol, after placebo inhalation, which was similar to that measured before the trial (0.04: 0.02‐0.09 mumol). 4. Both nedocromil sodium (4 mg) and sodium cromoglycate (10 mg) gave significant protection (P less than 0.05) against bradykinin‐induced bronchoconstriction (PD40 0.37: 0.19‐0.72 mumol after nedocromil sodium and 0.22: 0.11‐0.49 after sodium cromoglycate). 5. Since bradykinin‐induced bronchoconstriction is probably neurally mediated we conclude that both nedocromil sodium and sodium cromoglycate have an action on neural pathways which may be useful in the control of asthma symptoms.