Effects of dietary salt intake on plasma arginine

Citation
C. Kitiyakara et al., Effects of dietary salt intake on plasma arginine, AM J P-REG, 280(4), 2001, pp. R1069-R1075
Citations number
37
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
280
Issue
4
Year of publication
2001
Pages
R1069 - R1075
Database
ISI
SICI code
0363-6119(200104)280:4<R1069:EODSIO>2.0.ZU;2-5
Abstract
Because L-arginine is degraded by hepatic arginase to ornithine and urea an d is transported by the regulated 2A cationic amino acid y(+) transporter ( CAT2A), hepatic transport may regulate plasma arginine concentration. Group s 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 plasm a arginine concentration and renal nitric oxide (NO) generation by measurin g plasma arginine and ornithine concentrations, renal NO excretion, and exp ression of hepatic CAT2A, and arginase. LS rats had lower excretion of NO m etabolites and cGMP, lower plasma arginine concentration (LS: 83 +/- 7 vs. HS: 165 +/- 10 mu mol/1, P < 0.001), but higher plasma ornithine concentrat ion (LS: 82 6 6 vs. HS: 66 +/- 4 <mu>mol/1, P < 0.05) and urea excretion. H owever, neither the in vitro hepatic arginase activity nor the mRNA for hep atic arginase I was different between groups. In contrast, LS rats had twic e 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 pl asma ornithine concentration and urea excretion during LS indicates increas ed arginine metabolism by arginase. This cannot be ascribed to changes in h epatic arginase expression but may be a consequence of increased hepatic ar ginine uptake via CAT2A.