Tachykinins mediate the potentiation of antigen-induced bronchoconstriction by cold air in guinea pigs

The role of tachykinins in the potentiation of antigen-evoked bronchoconstriction induced by inhalation of cold air was studied in guinea pigs. Cold air was delivered through a tracheal cannula to anethetized, artificially ventilated guinea pigs sensitized with ovalbumin and pretreated with atropine (1.4 mu mol/kg). Inhalation of cold air increased total pulmonary resistance (R(L)) in a time-dependent manner; inhalation of cold air for 10 or 15 minutes, but not for 5 minutes, produced a significant increase in R(L). Aerosolized ovalbumin (5 breaths) increased R(L) in a dose-dependent manner (0.5% to 5%). Inhalation of cold air for 5 minutes significantly enhanced both the peak and the duration of the increased in R(L) induced by 0.5% ovalbumin. The tachykinin neurokinin 2-receptor antagonist, SR 48968 (0.3 mu mol/kg intravenously) inhibited both the peak and the duration of the bronchoconstriction induced by 5-minute inhibited of cold air and ovalbumin (0.5%), whereas it did not affect the response to ovalbumin (0.5%) alone. These findings suggest that exposure to cold air potentiates the bronchoconstriction response to antigen and that this potentiation is mediated by tachykinin release from sensory nerves.