Arginine (ARG) is the precursor of nitric oxide (NO), a potent vasodil
ator. Arginase (ASE) is released following hepatocellular damage, resu
lting in low plasma ARG levels. The effect of ASE infusion on hemodyna
mics was studied. Rats received a 20 min ASE or saline infusion, and s
ystemic hemodynamics and organ blood flow were studied, at 30 and 270
min, using radiolabeled microspheres. Compared with control, ASE resul
ted (30 min) in 1) undetectable ARG levels; 2) higher mean arterial pr
essure and total peripheral resistance (both p < .05); 3) higher blood
flow to the heart, kidneys, stomach, small intestine tall p < .05), a
nd spleen (p < .001); and 4) lower vascular resistance in the heart, k
idneys, stomach, and small intestine tall p < .05) and in the spleen (
p < .005), At 270 min, ASE rats had similar organ blood flow and highe
r nitrate levels in urine and plasma (both p < .05) compared with cont
rol. We conclude that ASE reduces ARG levels with simultaneous increas
e in mean arterial pressure and total peripheral resistance. Higher ni
trate production, suggesting higher NO formation in the presence of lo
w ARG plasma levels, is paradoxical but could explain the higher blood
flow in some organs, The increased total peripheral resistance during
higher nitrate formation suggests regional differences in dependency
of NO production on plasma ARG levels.