INCREASED L-ARGININE TRANSPORT IN HUMAN ERYTHROCYTES IN CHRONIC HEART-FAILURE

Citation
H. Hanssen et al., INCREASED L-ARGININE TRANSPORT IN HUMAN ERYTHROCYTES IN CHRONIC HEART-FAILURE, Clinical science, 94(1), 1998, pp. 43-48
Citations number
25
Categorie Soggetti
Medicine, Research & Experimental
Journal title
ISSN journal
01435221
Volume
94
Issue
1
Year of publication
1998
Pages
43 - 48
Database
ISI
SICI code
0143-5221(1998)94:1<43:ILTIHE>2.0.ZU;2-I
Abstract
1. Transport of L-arginine was investigated under zero-trans condition s in human erythrocytes from healthy donors and patients with heart fa ilure. 2. Saturable influx of L-arginine was mediated by the classical cationic amino acid transport systems y(+) and y(+)L. 3. The V-max fo r L-arginine transport via system y(+) increased from 292 to 490 mu mo l h(-1)1(-1) of cells in heart failure. 4. With system y(+) inhibited by N-ethylmaleimide (0.2 mmol/l), the V-max for the transport of L-arg inine via system y(+)L was unaffected in erythrocytes from patients wi th heart failure. 5. The inhibition of L-arginine and L-leucine influx by N-G-monomethyl-L-arginine was similar in erythrocytes from control and heart failure patients. 6. Plasma L-arginine levels were reduced in patients with heart failure (59 mu mol/l) compared with controls (1 25 mu mol/l). Plasma from patients with heart failure also contained t he endogenous L-arginine analogue N-G-monomethyl-L-arginine, which was undetectable in plasma from controls. 7. Intracellular concentrations of L-arginine and N-G-monomethyl-L-arginine were significantly elevat ed in erythrocytes from patients with heart failure compared with cont rols, consistent with an increased transport capacity for L-arginine a nd N-G-monomethyl-L-arginine. 8. The present study provides the first evidence that system y(+) mediates the increased transport of L-argini ne in human erythrocytes from patients with chronic heart failure. The se findings are similar to our previous results obtained in patients w ith chronic renal failure. Since both pathologies seem to present with an increased synthesis of nitric oxide, studies of L-arginine transpo rt in erythrocytes may provide a valuable paradigm to study abnormalit ies of the L-arginine-nitric oxide signalling pathway.