Document Detail

Arginase inhibition increases nitric oxide production in bovine pulmonary arterial endothelial cells.
MedLine Citation:
PMID:  14977627     Owner:  NLM     Status:  MEDLINE    
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.
Louis G Chicoine; Michael L Paffett; Tamara L Young; Leif D Nelin
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Publication Detail:
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:
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:
Created Date:  2004-06-09     Completed Date:  2004-07-08     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L60-8     Citation Subset:  IM    
Vascular Physiology Group and Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque 87131, USA.
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MeSH Terms
Arginase / antagonists & inhibitors*,  genetics,  metabolism
Arginine / pharmacokinetics,  pharmacology
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
Reg. No./Substance:
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

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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