Document Detail


Amino acids as modulators of endothelium-derived nitric oxide.
MedLine Citation:
PMID:  16571593     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To examine the mechanisms whereby amino acids modulate nitric oxide (NO) production and blood flow in the renal vasculature, chemiluminescence techniques were used to quantify NO in the renal venous effluent of the isolated, perfused rat kidney as different amino acids were added to the perfusate. The addition of 10(-4) or 10(-3) M cationic amino acids (l-ornithine, l-lysine, or l-homoarginine) or neutral amino acids (l-glutamine, l-leucine, or l-serine) to the perfusate decreased NO and increased renal vascular resistance. Perfusion with anionic amino acids (l-glutamate or l-aspartate) had no effect on either parameter. The effects of the cationic and neutral amino acids were reversed with 10(-3) M l-arginine and prevented by deendothelialization or NO synthase inhibition. The effects of the neutral amino acids but not the cationic amino acids were dependent on extracellular sodium. Cationic and neutral amino acids also decreased calcimycin-induced NO, as assessed by DAF-FM-T fluorescence, in cultured EA.hy926 endothelial cells. Inhibition of system y(+) or y(+)L by siRNA for the cationic amino acid transporter 1 or the CD98/4F2 heavy chain diminished the NO-depleting effects of these amino acids. Finally, transport studies in cultured cells demonstrated that cationic or neutral amino acids in the extracellular space stimulate efflux of l-arginine out of the cell. Thus the present experiments demonstrate that cationic and neutral amino acids can modulate NO production in endothelial cells by altering cellular l-arginine transport through y(+) and y(+)L transport mechanisms.
Authors:
Masao Kakoki; Hyung-Suk Kim; Cora-Jean S Edgell; Nobuyo Maeda; Oliver Smithies; David L Mattson
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-03-28
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  291     ISSN:  1931-857X     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-07-07     Completed Date:  2006-08-28     Revised Date:  2011-04-28    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F297-304     Citation Subset:  IM    
Affiliation:
Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, USA.
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MeSH Terms
Descriptor/Qualifier:
Amino Acids / physiology*
Animals
Antigens, CD98 Heavy Chain / pharmacology
Arginine / metabolism*
Biological Transport / drug effects,  physiology
Cationic Amino Acid Transporter 1 / genetics
Cell Line
Endothelium, Vascular / chemistry,  metabolism*
Enzyme Inhibitors / pharmacology
Humans
Kidney / blood supply,  physiology
Male
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide / analysis,  metabolism*
RNA, Small Interfering / genetics,  pharmacology
Rats
Rats, Sprague-Dawley
Vascular Resistance / drug effects,  physiology
Grant Support
ID/Acronym/Agency:
DK-62803/DK/NIDDK NIH HHS; HL-29587/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Amino Acids; 0/Antigens, CD98 Heavy Chain; 0/Cationic Amino Acid Transporter 1; 0/Enzyme Inhibitors; 0/RNA, Small Interfering; 10102-43-9/Nitric Oxide; 50903-99-6/NG-Nitroarginine Methyl Ester; 74-79-3/Arginine

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


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