| pubmed-article:10952667 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10952667 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:10952667 | lifeskim:mentions | umls-concept:C0458827 | lld:lifeskim |
| pubmed-article:10952667 | lifeskim:mentions | umls-concept:C1149793 | lld:lifeskim |
| pubmed-article:10952667 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:10952667 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:10952667 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
| pubmed-article:10952667 | lifeskim:mentions | umls-concept:C0599668 | lld:lifeskim |
| pubmed-article:10952667 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:10952667 | pubmed:dateCreated | 2000-10-5 | lld:pubmed |
| pubmed-article:10952667 | pubmed:abstractText | 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. | lld:pubmed |
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| pubmed-article:10952667 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10952667 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10952667 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10952667 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:10952667 | pubmed:issn | 0007-1188 | lld:pubmed |
| pubmed-article:10952667 | pubmed:author | pubmed-author:ZaagsmaJJ | lld:pubmed |
| pubmed-article:10952667 | pubmed:author | pubmed-author:MeursHH | lld:pubmed |
| pubmed-article:10952667 | pubmed:author | pubmed-author:BoucherJ LJL | lld:pubmed |
| pubmed-article:10952667 | pubmed:author | pubmed-author:PetheSS | lld:pubmed |
| pubmed-article:10952667 | pubmed:author | pubmed-author:Vadon-Le... | lld:pubmed |
| pubmed-article:10952667 | pubmed:author | pubmed-author:HamerM AMA | lld:pubmed |
| pubmed-article:10952667 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10952667 | pubmed:volume | 130 | lld:pubmed |
| pubmed-article:10952667 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10952667 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10952667 | pubmed:pagination | 1793-8 | lld:pubmed |
| pubmed-article:10952667 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10952667 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10952667 | pubmed:articleTitle | Modulation of cholinergic airway reactivity and nitric oxide production by endogenous arginase activity. | lld:pubmed |
| pubmed-article:10952667 | pubmed:affiliation | Department of Molecular Pharmacology, University Centre for Pharmacy, A. Deusinglaan 1, 9713 AV Groningen, The Netherlands. | lld:pubmed |
| pubmed-article:10952667 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10952667 | pubmed:publicationType | In Vitro | lld:pubmed |
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