Bradykinin, 10 to 1000 mu g given by aerosol into the nasal cavity of
normal, healthy volunteers, produced a dose-related increase of nasal
airway resistance. Bradykinin also reduced the minimal nasal cross-sec
tional area (A,,,), increased albumin release into nasal lavage fluid
and increased the symptoms of nasal inflammation. Pretreatment with ce
tirizine (10 mg orally) reduced the fall in A(min) induced by bradykin
in, 300 mu g, but not by bradykinin, 100 mu g. Pre-treatment of the su
bjects with the H-1 histamine receptor antagonist cetirizine (10 mg, o
rally) or terfenadine (60 mg, orally) 3 h before bradykinin administra
tion caused significant reduction of the bradykinin-induced increase i
n nasal airway resistance in the upper range of bradykinin doses (300-
1000 mu g) but not in the lower range (10-100 mu g). Cetirizine reduce
d the albumin release into the nasal airway and the symptoms induced b
y bradykinin, 1000 mu g. Following nasal challenge with bradykinin 300
mu g or 1000 mu g, no increase could be detected in the histamine con
tent of nasal lavage fluid. Isolated human nasal cells released histam
ine in response to bradykinin, 33 and 100 mu M, anti-IgE and calcium i
onophore, A23187. We conclude that the actions of bradykinin in the hu
man nasal airway are, in part, accounted for by the release of histami
ne.