ArticleBritish journal of pharmacology2000
Modulation of cholinergic airway reactivity and nitric oxide production by endogenous arginase activity.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 66 citations in OpenAlex.
- Effect of Anti-IL17 Antibody Treatment Alone and in Combination With Rho-Kinase Inhibitor in a Murine Model of Asthma.Frontiers in physiology · 2018Article
- Modulation of the oscillatory mechanics of lung tissue and the oxidative stress response induced by arginase inhibition in a chronic allergic inflammation model.BMC pulmonary medicine · 2013Article
- Competitive metabolism of L-arginine: arginase as a therapeutic target in asthma.Journal of biomedical research · 2011Article
- Arginase and arginine dysregulation in asthma.Journal of allergy · 2011Article
- Species differences in expression pattern of arginase isoenzymes and differential effects of arginase inhibition on collagen synthesis in human and rat pulmonary fibroblasts.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
- Arginase inhibition in airways from normal and nitric oxide synthase 2-knockout mice exposed to ovalbumin.Toxicology and applied pharmacology · 2010Article
- Arginase: a key enzyme in the pathophysiology of allergic asthma opening novel therapeutic perspectives.British journal of pharmacology · 2009Review
- Article
- Arginase and pulmonary diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2008Review
- Arginase modulates myocardial contractility by a nitric oxide synthase 1-dependent mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Arginase strongly impairs neuronal nitric oxide-mediated airway smooth muscle relaxation in allergic asthma.Respiratory research · 2006Article
- Arginase attenuates inhibitory nonadrenergic noncholinergic nerve-induced nitric oxide generation and airway smooth muscle relaxation.Respiratory research · 2005Article
- Heparin normalizes allergen-induced nitric oxide deficiency and airway hyperresponsiveness.British journal of pharmacology · 2004Article
- Glucocorticoid inhibition of interleukin-4 (IL-4) and interleukin-13 (IL-13) induced up-regulation of arginase in rat airway fibroblasts.Naunyn-Schmiedeberg's archives of pharmacology · 2003Article
- Increased arginase activity underlies allergen-induced deficiency of cNOS-derived nitric oxide and airway hyperresponsiveness.British journal of pharmacology · 2002Article
- Role of nitric oxide and superoxide in allergen-induced airway hyperreactivity after the late asthmatic reaction in guinea-pigs.British journal of pharmacology · 2001Article
- Glucocorticoids inhibit lipopolysaccharide-induced up-regulation of arginase in rat alveolar macrophages.British journal of pharmacology · 2001Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholinergic airway constriction is functionally antagonized by agonist-induced constitutive nitric oxide synthase (cNOS)-derived nitric oxide (NO). Since cNOS and arginase, which hydrolyzes L-arginine to L-ornithine and urea, use L-arginine as a common substrate, competition between both enzymes for the substrate could be involved in the regulation of cholinergic airway reactivity. Using a perfused guinea-pig tracheal tube preparation, we investigated the modulation of methacholine-induced airway constriction by the recently developed, potent and specific arginase inhibitor N(Omega)-hydroxy-nor-L-arginine (nor-NOHA). Intraluminal (IL) administration of nor-NOHA caused a concentration-dependent inhibition of the maximal effect (E(max)) in response to IL methacholine, which was maximal in the presence of 5 microM nor-NOHA (E(max)=31.2+/-1.6% of extraluminal (EL) 40 mM KCl-induced constriction versus 51.6+/-2.1% in controls, P<0.001). In addition, the pEC(50) (-log(10) EC(50)) was slightly but significantly reduced in the presence of 5 microM nor-NOHA. The inhibition of E(max) by 5 microM nor-NOHA was concentration-dependently reversed by the NOS inhibitor N(Omega)-nitro-L-arginine methyl ester (L-NAME), reaching an E(max) of 89.4+/-7.7% in the presence of 0.5 mM L-NAME (P<0.01). A similar E(max) in the presence of 0.5 mM L-NAME was obtained in control preparations (85.2+/-9.7%, n.s.). In the presence of excess of exogenously applied L-arginine (5 mM), 5 microM nor-NOHA was ineffective (E(max)=33.1+/-5.8 versus 31.1+/-7.5% in controls, n.s.). The results indicate that endogenous arginase activity potentiates methacholine-induced airway constriction by inhibition of NO production, presumably by competition with cNOS for the common substrate, L-arginine. This finding may represent an important novel regulation mechanism of airway reactivity.
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