Increased cationic amino acid flux through a newly expressed transporter in cells overproducing nitric oxide from patients with septic shock

Reade, Michael C., Clark, Megan F., Young, J. Duncan and Boyd, C. A. R. (2002) Increased cationic amino acid flux through a newly expressed transporter in cells overproducing nitric oxide from patients with septic shock. Clinical Science, 102 6: 645-650. doi:10.1042/CS20010329


Author Reade, Michael C.
Clark, Megan F.
Young, J. Duncan
Boyd, C. A. R.
Title Increased cationic amino acid flux through a newly expressed transporter in cells overproducing nitric oxide from patients with septic shock
Journal name Clinical Science   Check publisher's open access policy
ISSN 0143-5221
1470-8736
Publication date 2002-06-01
Year available 2002
Sub-type Article (original research)
DOI 10.1042/CS20010329
Open Access Status Not yet assessed
Volume 102
Issue 6
Start page 645
End page 650
Total pages 6
Place of publication London, United Kingdom
Publisher Portland Press
Language eng
Formatted abstract
Increased production of nitric oxide (NO) is thought to be a factor in the pathogenesis of many human diseases - among them the hypotension that often accompanies sepsis. The supply of the cationic amino acid arginine is known to be rate-limiting for NO production. We hypothesized that cationic amino acid transport might be increased in cells producing excess NO from patients with septic shock. Peripheral blood mononuclear cells were isolated from patients with sepsis and from healthy control subjects. The rates of both NO production and cationic amino acid uptake were increased in cells from patients with septic shock. The increased transport was due almost entirely to an increase in the activity of one transporter, subtype y+. The activity of the other major cationic amino acid transporter (y+L) was unchanged. The expression of CAT2 mRNA, which encodes a y+ transporter protein, was also increased in these cells. We suggest that CAT2 might be a therapeutic target to prevent excess NO production in sepsis and possibly other human disease states, while leaving basal production unchanged.
Keyword Arginine
CAT2
Nitric oxide
Sepsis
Septic shock
Y+
Y+L
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
 
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