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Deficiency of nitric oxide in polycation-induced airway hyperreactivity
Deficiency of nitric oxide in polycation-induced airway hyperreactivity
- Source :
- British Journal of Pharmacology. 126:559-562
- Publication Year :
- 1999
- Publisher :
- Wiley, 1999.
-
Abstract
- Using a perfused guinea-pig tracheal tube preparation, we investigated the role of endogenous nitric oxide (NO) in polycation-induced airway hyperreactivity (AHR) to methacholine. Intraluminal (IL) administration of the NO synthase inhibitor Nω-nitro-L-arginine methyl ester (L-NAME; 100 μM) caused a 1.8 fold increase in the maximal contractile response (Emax) to IL methacholine compared to control, without an effect on the pEC50 (−log10 EC50). The polycation poly-L-arginine (100 μg ml−1, IL) similarly enhanced the Emax for methacholine; however, the pEC50 value was also increased, by one log10 unit. L-NAME had no effect on the enhanced methacholine response of poly-L-arginine-treated airways, while the enhanced agonist response was completely normalized by the polyanion heparin (25 u ml−1, IL). In addition, the effect of L-NAME was fully restored in the poly-L-arginine plus heparin treated airways. The results indicate that, in addition to enhanced epithelial permeability, a deficiency of endogenous NO contributes to polycation-induced AHR. The latter finding may represent a novel mechanism of AHR induced by eosinophil-derived cationic proteins in allergic asthma. British Journal of Pharmacology (1999) 126, 559–562; doi:10.1038/sj.bjp.0702372
Details
- ISSN :
- 00071188
- Volume :
- 126
- Database :
- OpenAIRE
- Journal :
- British Journal of Pharmacology
- Accession number :
- edsair.doi...........2367f3cf5a52922a1d28a0ee1dd95a6e
- Full Text :
- https://doi.org/10.1038/sj.bjp.0702372