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Prostaglandins mediate bradykinin-induced reduction of exhaled nitric oxide in asthma.
Eur Respir J. 1999 Nov; 14(5):1023-7.ER

Abstract

Bradykinin (BK) is a mediator of inflammation in asthma with potent bronchoconstrictor actions. Endogenous release of nitric oxide may inhibit BK-induced bronchoconstriction. This study investigated whether bradykinin inhalation could modulate exhaled NO levels in normal and asthmatic subjects, and whether the bradykinin-induced effects were mediated through the production of cyclo-oxygenase products in patients with asthma, by studying the effect of the cyclo-oxygenase inhibitor, L-acetylsalicylic acid (L-ASA). Exhaled NO concentration and forced expiratory volume in one second (FEV1) were measured by chemiluminescence following inhalation of increasing concentrations of BK. In asthmatics (n=11), BK induced a dose-dependent decrease in exhaled NO concentration from 21.3+/-1.6 to 6.+/-0.5 parts per billion (ppb) (p<0.01) at the highest concentration, associated with a significant fall in FEV1. In normal subjects (n=10), the exhaled NO concentration fell from 7.2+/-0.13 to 4.3+/-0.51 ppb (p<0.001) 15 min, after a single inhalation of BK, but without a significant change in FEV1. In asthmatic subjects, pretreatment with inhaled L-ASA (90 x mg x mL(-1), 4 mL) did not alter exhaled NO levels, but prevented a BK-induced fall in exhaled NO concentration, as indicated by a significant increase in exhaled NO levels at the provocative concentration of BK causing a 20% fall in FEV1, (5.7 +/- 0.94 ppb after placebo and 12.0 +/- 1.8 ppb after L-ASA; p<0.05). L-ASA significantly reduced bronchial responsiveness to BK 3.9-fold (p<0.01). Inhaled bradykinin induced bronchoconstriction and a reduction in exhaled nitric oxide levels in asthmatic subjects, an effect that is partly mediated by cyclo-oxygenase products.

Authors+Show Affiliations

Dept of Thoracic Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London, UK.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10596684

Citation

Kharitonov, S A., et al. "Prostaglandins Mediate Bradykinin-induced Reduction of Exhaled Nitric Oxide in Asthma." The European Respiratory Journal, vol. 14, no. 5, 1999, pp. 1023-7.
Kharitonov SA, Sapienza MM, Chung KF, et al. Prostaglandins mediate bradykinin-induced reduction of exhaled nitric oxide in asthma. Eur Respir J. 1999;14(5):1023-7.
Kharitonov, S. A., Sapienza, M. M., Chung, K. F., & Barnes, P. J. (1999). Prostaglandins mediate bradykinin-induced reduction of exhaled nitric oxide in asthma. The European Respiratory Journal, 14(5), 1023-7.
Kharitonov SA, et al. Prostaglandins Mediate Bradykinin-induced Reduction of Exhaled Nitric Oxide in Asthma. Eur Respir J. 1999;14(5):1023-7. PubMed PMID: 10596684.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prostaglandins mediate bradykinin-induced reduction of exhaled nitric oxide in asthma. AU - Kharitonov,S A, AU - Sapienza,M M, AU - Chung,K F, AU - Barnes,P J, PY - 1999/12/22/pubmed PY - 1999/12/22/medline PY - 1999/12/22/entrez SP - 1023 EP - 7 JF - The European respiratory journal JO - Eur. Respir. J. VL - 14 IS - 5 N2 - Bradykinin (BK) is a mediator of inflammation in asthma with potent bronchoconstrictor actions. Endogenous release of nitric oxide may inhibit BK-induced bronchoconstriction. This study investigated whether bradykinin inhalation could modulate exhaled NO levels in normal and asthmatic subjects, and whether the bradykinin-induced effects were mediated through the production of cyclo-oxygenase products in patients with asthma, by studying the effect of the cyclo-oxygenase inhibitor, L-acetylsalicylic acid (L-ASA). Exhaled NO concentration and forced expiratory volume in one second (FEV1) were measured by chemiluminescence following inhalation of increasing concentrations of BK. In asthmatics (n=11), BK induced a dose-dependent decrease in exhaled NO concentration from 21.3+/-1.6 to 6.+/-0.5 parts per billion (ppb) (p<0.01) at the highest concentration, associated with a significant fall in FEV1. In normal subjects (n=10), the exhaled NO concentration fell from 7.2+/-0.13 to 4.3+/-0.51 ppb (p<0.001) 15 min, after a single inhalation of BK, but without a significant change in FEV1. In asthmatic subjects, pretreatment with inhaled L-ASA (90 x mg x mL(-1), 4 mL) did not alter exhaled NO levels, but prevented a BK-induced fall in exhaled NO concentration, as indicated by a significant increase in exhaled NO levels at the provocative concentration of BK causing a 20% fall in FEV1, (5.7 +/- 0.94 ppb after placebo and 12.0 +/- 1.8 ppb after L-ASA; p<0.05). L-ASA significantly reduced bronchial responsiveness to BK 3.9-fold (p<0.01). Inhaled bradykinin induced bronchoconstriction and a reduction in exhaled nitric oxide levels in asthmatic subjects, an effect that is partly mediated by cyclo-oxygenase products. SN - 0903-1936 UR - https://www.unboundmedicine.com/medline/citation/10596684/Prostaglandins_mediate_bradykinin_induced_reduction_of_exhaled_nitric_oxide_in_asthma_ L2 - http://erj.ersjournals.com/cgi/pmidlookup?view=long&amp;pmid=10596684 DB - PRIME DP - Unbound Medicine ER -