Research LettersImpairment of bronchoprotection by nitric oxide in severe asthma
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Nitric Oxide and Nitrogen Oxides
2021, Encyclopedia of Respiratory Medicine, Second EditionBradykinin in asthma: Modulation of airway inflammation and remodelling
2018, European Journal of PharmacologyCitation Excerpt :On the other hand, epithelium-derived bronchoprotective factors such as nitric oxide are released by bradykinin (Figini et al., 1996; Ricciardolo et al., 2000) negatively modulating enhanced bronchial hyperresponsiveness in mild asthma (Ricciardolo et al., 1996, 2001) (Fig. 1). A further study also showed the impairment of the bronchoprotective nitric oxide on the bradykinin-induced airway hyperresponsiveness in moderate-to-severe asthma suggesting the loss of this protective mechanism in difficult-to-control patients (Ricciardolo et al., 1997). In addition, clinical studies confirmed the role of corticosteroids in decreasing bronchial hyperresponsiveness to bradykinin and the bradykinin receptor expression in eosinophils/neutrophils from asthmatics in association with the improvement of respiratory symptoms (Bertram et al., 2007, 2009; Reynolds et al., 2002) indicating that the bradykinin-induced effects on the asthmatic airways seem to be corticosteroid sensitive.
Effect of 45nm silver nanoparticles (AgNPs) upon the smooth muscle of rat trachea: Role of nitric oxide
2011, Toxicology LettersCitation Excerpt :The neuronal (nNOS) and endothelial (eNOS) are considered constitutive and are involved in vaso and bronchodilation (Courtois et al., 2008; Prado et al., 2006; Hasaneen et al., 2003). The inducible NOS (iNOS) is stimulated and produces NO in large amounts by many pro-inflammatory cytokines and is expressed in several types of inflammatory tissues (Ricciardolo, 1997; Ricciardolo et al., 2004). It is known that excessive NO produced mainly by iNOS is responsible for the development of many respiratory diseases and their symptoms include bronchial hyper-reactivity (Antošová et al., 2006).
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