PROSTAGLANDIN-F-2-ALPHA ENHANCEMENT OF CAPSAICIN INDUCED COUGH IN MAN - MODULATION BY BETA-2-ADRENERGIC AND ANTICHOLINERGIC DRUGS

The effect of inhaled prostaglandin (PG) F(2α) on the response to the inhaled tussive agent capsaicin was investigated in normal subjects. Seven subjects inhaled three breaths of four doses of capsaicin (0.3, 0.6, 1.2, and 2.4 nmol) before and immediately after inhaling PGF(2α) (0.1 μmol) or placebo (0.15M NaCl) on separate days. The numbers of capsaicin induced coughs were greater after PGF(2α) (mean 42.3 coughs) than after 0.15M sodium chloride (30.1). Visual analogue scores (0-10 on a 10 cm continuous scale) showed that capsaicin was more irritant after PGF(2α) than after saline. Total respiratory resistance Rrs), measured by the forced oscillation technique, was unaltered throughout the study. A double blind, placebo controlled study of the effects of inhaled salbutamol (200 μg, 0.6 μmol) and ipratropium bromide (40 μg, 0.1 μmol) on cough induced by capsaicin (2.4 nmol) and by PGF(2α) (0.1 μmol) and on PGF(2α) augmented, capsaicin induced coughing was performed in seven subjects. Neither drug had any effect on capsaicin induced coughing. Salbutamol reduced coughing due to PGF(2α) (mean 7.7 coughs after salbutamol, 9.3 after placebo) but ipratropium bromide did not (mean 6.9 coughs after ipratropium bromide, 6.6 after placebo). Salbutamol also inhibited the augmentation of the capsaicin induced cough that followed inhalation of PGF(2α) (mean augmentation 1.9 coughs after salbutamol, 4.1 after placebo), whereas ipratropium bromide did not (augmentation 1.7 coughs after ipratropium bromide, 2.7 after placebo). No changes in Rrs were seen after PGF(2α) or either drug. Thus salbutamol reduces PGF(2α) induced cough and the augmentation of capsaicin induced cough that follows PGF(2α).