Evidence for reduction of bradykinin-induced bronchoconstriction in guinea-pigs by release of nitric oxide

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Abstract
1 In this study the influence of nitric oxide (NO) on the bronchoconstriction induced by bradykinin in anaesthetized and artifically ventilated guinea-pigs pretreated with atropine was investigated. 2 Aerosol administration of bradykinin (0.1 −1 mm, 40 breaths) caused a dose-dependent increase in lung resistance (R1): maximum increase in R1 was 2.5 fold the baseline value. Pretreatment with aerosolized NG-nitro-1-arginine methyl ester (1-NAME) or NG-monomethyl-1-arginine (1-NMMA) (1 mm, 10 breaths every 5min for 30min), NO synthase inhibitors, markedly increased the bron-choconstrictor response to bradykinin. 1-Arginine, but not D-arginine, (3 mm, 10 breaths every 5 min for 30 min) reversed the hyperresponsiveness to aerosolized bradykinin caused by 1-NAME and 1-NMMA. 3 1-NAME (1 mm, 10 breaths every 5 min for 30 min) increased the bronchoconstriction induced by intravenous bradykinin (1-10nmol kg1). 1-Arginine, but not D-arginine, (10 breaths every 5 min for 30 min) reversed the hyperresponsiveness to intravenous bradykinin caused by 1-NAME. 4 The increase in RL induced by capsaicin, either aerosol (10 μm, 10 breaths) or i.v. (20 nmol kg−1) was not affected by 1-NAME (1 mm, 10 breaths every 5 min for 30 min). Acute resection of the vagi did not affect the bronchoconstriction evoked by bradykinin in guinea-pigs, either in the absence or presence of 1-NAME (1 mm, 10 breaths every 5 min for 30 min). 4 These results suggest that, irrespective of the route of administration, bradykinin releases NO or a related molecule which exerts a bronchodilator action that opposes the bronchoconstrictor mechanisms activated by bradykinin itself.