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.