1. The aim of this study was to investigate the action of bradykinin on resistance to airflow and on vascular permeability in the human nasal airway, and to explore the receptor mediating these effects. 2. Aerosol administration of bradykinin (10-1000 micrograms) caused a dose-related increase in nasal airway resistance (NAR) and an increase in albumin content of nasal lavage. 3. The bradykinin antagonists, [1-adamantane acetyl-D-Arg0, Hyp3, Thi5,8, D-Phe7]-bradykinin, 100 micrograms, and [D-Arg0, Hyp3, Thi5, D-Tic7, Oic8]-bradykinin, 100 micrograms, given 2 min before bradykinin, inhibited the increase in NAR and the increase of albumin content of nasal lavage caused by bradykinin. 4. The bradykinin antagonist, [D-Arg0, Hyp3, D-Phe7]-bradykinin (100 micrograms) did not affect the increase in NAR produced by bradykinin, or the albumin content of nasal lavage. Increasing the dose of the antagonist to 1000 micrograms did not change the increase in NAR induced by bradykinin. 5. The selective B1 kinin receptor agonist, [Des-Arg10]-kallidin (100 micrograms) did not affect NAR or the albumin content of nasal lavage. 6. The receptor mediating increased NAR and the release of albumin induced by bradykinin in the human nasal airway appears not to be a B1 kinin receptor. The data are not entirely consistent with the effects of bradykinin in the human nasal airway being mediated by a B2 kinin receptor.