Fig. 6.

Three days after ozone, vagally mediated hyperreactivity is mediated by NK₁ receptors. Electrical stimulation of both vagus nerves produced frequency-dependent bronchoconstriction (A, ○) that was significantly potentiated 3 days after a single exposure to ozone (A, ●). The NK₁ receptor antagonist CP-96,345 (3 mg/kg iv) prevented ozone-induced hyperreactivity (A, ▴). Bronchoconstriction induced by both acetylcholine (B) and methacholine (C) was potentiated by ozone (●) but was not inhibited by the NK₁ receptor antagonist (▴). Treatment of air-exposed controls with the NK₁ receptor antagonist had no effect on vagally, acetylcholine-, or methacholine-induced bronchoconstriction (A–C, ▵). *Significantly different from air controls. †Significantly different from ozone. Data are expressed as means ± SE, n = 4–12.