Characterization of cationic amino acid transport systems in rat erythrocytes: Lack of effect of uraemia on L-arginine influx

1. Chronic renal failure (CRF) is associated with the abnormal regulation of nitric oxide (NO) synthesis at the systemic level. The transport of L-arginine, upregulated in blood cells from uraemic patients, modulates NO synthesis in this pathological condition. The model of partial nephrectomy in rats is widely accepted as a valid model of uraemia. Because there are no reports of L-arginine transport in blood cells from uraemic rats, the aim of the present study was to investigate L-arginine transport in red blood cells (RBCs) from these rats. 2. The kinetics of L-arginine transport in RBC and plasma and the amino acid profiles of RBC were investigated in control, sham-operated and subtotally nephrectomized rats. 3. L-Arginine transport was mediated via the cationic amino acid transport system y + and a transport system with kinetics resembling the human system y + L. In control RBC, the apparent K i for L-leucine inhibition of L-arginine transport via system y + L was 0.16 ± 0.02 and 4.8 ± 2 mmol/L in the presence of Li + and Na + , respectively. 4. The V max values for L-arginine transport via system y + L and system y + were similar in RBC from control sham-operated and uraemic rats. Moreover, L-arginine concentrations in plasma and RBC were not affected by uraemia. 5. The findings of the present study provide the first evidence that L-arginine transport in rat erythrocytes is mediated by two distinct cationic transport systems with characteristics of systems y + and y + L, which accept neutral amino acids only in the presence of Li + . In contrast with previous studies in uraemic patients, plasma levels and maximal transport rates of L-arginine were not altered in this rat model of CRF.