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Division of Nephrology and Hypertension, Departments of 1 Medicine and 2 Pediatrics, Georgetown University Center for Hypertension and Renal Disease Research, Washington, District of Columbia 20007
Because L-arginine is degraded by hepatic arginase to ornithine and urea and is transported by the regulated 2A cationic amino acid y+ transporter (CAT2A), hepatic transport may regulate plasma arginine concentration. Groups of rats (n = 6) were fed a diet of either low salt (LS) or high salt (HS) for 7 days to test the hypothesis that dietary salt intake regulates plasma arginine concentration and renal nitric oxide (NO) generation by measuring plasma arginine and ornithine concentrations, renal NO excretion, and expression of hepatic CAT2A, and arginase. LS rats had lower excretion of NO metabolites and cGMP, lower plasma arginine concentration (LS: 83 ± 7 vs. HS: 165 ± 10 µmol/l, P < 0.001), but higher plasma ornithine concentration (LS: 82 ± 6 vs. HS: 66 ± 4 µmol/l, P < 0.05) and urea excretion. However, neither the in vitro hepatic arginase activity nor the mRNA for hepatic arginase I was different between groups. In contrast, LS rats had twice the abundance of mRNA for hepatic CAT2A (LS: 3.4 ± 0.4 vs. HS: 1.6 ± 0.5, P < 0.05). The reduced plasma arginine concentration with increased plasma ornithine concentration and urea excretion during LS indicates increased arginine metabolism by arginase. This cannot be ascribed to changes in hepatic arginase expression but may be a consequence of increased hepatic arginine uptake via CAT2A.
nitric oxide; system y+ transport; cationic amino acid transporter; ornithine; urea
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