| Arginase inhibition increases nitric oxide production in bovine pulmonary arterial endothelial cells. | |
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MedLine Citation:
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PMID: 14977627 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Nitric oxide (NO) is produced by NO synthase (NOS) from L-arginine (L-Arg). Alternatively, L-Arg can be metabolized by arginase to produce L-ornithine and urea. Arginase (AR) exists in two isoforms, ARI and ARII. We hypothesized that inhibiting AR with L-valine (L-Val) would increase NO production in bovine pulmonary arterial endothelial cells (bPAEC). bPAEC were grown to confluence in either regular medium (EGM; control) or EGM with lipopolysaccharide and tumor necrosis factor-alpha (L/T) added. Treatment of bPAEC with L/T resulted in greater ARI protein expression and ARII mRNA expression than in control bPAEC. Addition of L-Val to the medium led to a concentration-dependent decrease in urea production and a concentration-dependent increase in NO production in both control and L/T-treated bPAEC. In a second set of experiments, control and L/T bPAEC were grown in EGM, EGM with 30 mM L-Val, EGM with 10 mM L-Arg, or EGM with both 10 mM L-Arg and 30 mM L-Val. In both control and L/T bPAEC, treatment with L-Val decreased urea production and increased NO production. Treatment with L-Arg increased both urea and NO production. The addition of the combination L-Arg and L-Val decreased urea production compared with the addition of L-Arg alone and increased NO production compared with L-Val alone. These data suggest that competition for intracellular L-Arg by AR may be involved in the regulation of NOS activity in control bPAEC and in response to L/T treatment. |
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Authors:
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Louis G Chicoine; Michael L Paffett; Tamara L Young; Leif D Nelin |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2004-02-20 |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 287 ISSN: 1040-0605 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2004 Jul |
Date Detail:
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Created Date: 2004-06-09 Completed Date: 2004-07-08 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L60-8 Citation Subset: IM |
Affiliation:
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Vascular Physiology Group and Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque 87131, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arginase / antagonists & inhibitors*, genetics, metabolism Arginine / pharmacokinetics, pharmacology Cattle Cells, Cultured Dose-Response Relationship, Drug Drug Combinations Endothelium, Vascular / cytology, metabolism* Isoenzymes / genetics, metabolism Lipopolysaccharides / pharmacology Nitrates / metabolism Nitric Oxide / biosynthesis* Nitrites / metabolism Osmolar Concentration Pulmonary Artery / cytology, metabolism* RNA, Messenger / metabolism Time Factors Tumor Necrosis Factor-alpha / pharmacology Urea / antagonists & inhibitors Valine / pharmacology* |
| Grant Support | |
ID/Acronym/Agency:
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HL-04050/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Drug Combinations; 0/Isoenzymes; 0/Lipopolysaccharides; 0/Nitrates; 0/Nitrites; 0/RNA, Messenger; 0/Tumor Necrosis Factor-alpha; 10102-43-9/Nitric Oxide; 57-13-6/Urea; 7004-03-7/Valine; 74-79-3/Arginine; EC 3.5.3.1/Arginase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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