Adenosine, a naturally occurring purine nucleoside, elicits dose-relat
ed bronchoconstriction in asthmatic subjects when administered by inha
lation and it is recovered in increased amounts from the bronchial lav
age fluid of subjects with active asthma when compared to normal contr
ols. Although the mechanism by which adenosine mediates bronchoconstri
ction in asthmatic subjects is not clear, recent data indicate an impo
rtant role for mast cell mediator release. We have recently shown that
local airway challenge with adenosine in subjects with asthma and rhi
nitis provokes an increase in the levels of PGD2, histamine and trypta
se. However, airway responsiveness and atopic status are the most impo
rtant determinants of adenosine-induced responses, regardless of any i
ncreases in mast cell mediators in airway fluids. New discoveries sugg
est that the airway response to adenosine may be an index of mast cell
priming and therefore may provide a useful tool to further explore th
e inflammatory processes in allergic asthma and rhinitis. Therefore ad
enosine provocation may gain increasing acceptance as an additional me
asure of disease activity in asthma and rhinitis.