Transport of extracellular l-arginine via cationic amino acid transporter is required during in vivo endothelial nitric oxide production.
Am J Physiol Heart Circ Physiol
; 289(4): H1381-90, 2005 Oct.
Article
em En
| MEDLINE
| ID: mdl-15849232
ABSTRACT
In cultured endothelial cells, 70-95% of extracellular l-arginine uptake has been attributed to the cationic amino acid transporter-1 protein (CAT-1). We tested the hypothesis that extracellular l-arginine entry into endothelial cells via CAT-1 plays a crucial role in endothelial nitric oxide (NO) production during in vivo conditions. Using l-lysine, the preferred amino acid transported by CAT-1, we competitively inhibited extracellular l-arginine transport into endothelial cells during conditions of NaCl hyperosmolarity, low oxygen, and flow increase. Our prior studies indicate that each of these perturbations causes NO-dependent vasodilation. The perivascular NO concentration ([NO]) and blood flow were determined in the in vivo rat intestinal microvasculature. Suppression of extracellular l-arginine transport significantly and strongly inhibited increases in vascular [NO] and intestinal blood flow during NaCl hyperosmolarity, lowered oxygen tension, and increased flow. These results suggest that l-arginine from the extracellular space is accumulated by CAT-1. When CAT-1-mediated transport of extracellular l-arginine into endothelial cells was suppressed, the endothelial cell NO response to a wide range of physiological stimuli was strongly depressed.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Arginina
/
Endotélio Vascular
/
Transportador 1 de Aminoácidos Catiônicos
/
Óxido Nítrico
Limite:
Animals
Idioma:
En
Revista:
Am J Physiol Heart Circ Physiol
Ano de publicação:
2005
Tipo de documento:
Article