Our earlier studies have shown development of indothelial dysfunction
in the feline renal artery during hemorrhagic hypotension. Because L-a
rginine (L-Arg), the precursor of nitric oxide (NO), reportedly improv
es endothelial function in several pathophysiological slates including
hypotension, we investigated its possible beneficial effect on the ad
renal and renal circulations during hemorrhagic hypotension in anesthe
tized, ventilated cats. Hypotension (mean arterial pressure 50 mm Hg)
significantly increased vascular resistance and decreased blood flow (
radiolabeled microspheres) in both adrenal and renal cortices. L-Arg (
30 mg/kg bolus, 10 mg/kg/min infusion, i.v.) had no significant hemody
namic effects in normotension but prevented the increase of the vascul
ar resistance and improved blood flow in the adrenal cortex during hyp
otension. In the kidney, L-Arg also prevented hemorrhage-induced vasoc
onstriction, although its effect on blood flow did not reach significa
nce. The NO synthase inhibitor N-G-nitro-L-arginine (30 mg/kg bolus, 1
mg/kg/min infusion, i.v.) increased adrenal and renal vascular resist
ances to a similar extent as that observed during hypotension. It thus
seems that an L-Arg-reversible dysfunction of the endothelial NO-synt
hesizing pathway contributes to hemorrhage-induced adrenal and renal v
asoconstriction.