TY - JOUR
T1 - Effect of L-arginine on adrenal and renal blood flows during hemorrhage in cats
AU - Benyo, Z.
AU - Szabo, C.
AU - Csaki, C.
AU - Wahl, M.
AU - Kovach, A. G.B.
AU - Sandor, P.
N1 - Funding Information:
This work was supported by grants from the Hungarian OTKA (F 013241, W 015186, and T 017790) and ETT (518/1996), by a grant of the National Institutes of Health (NS 10939-20), and by the German BMBF. Dr. Benyó is grateful for support from the Alexander von Humboldt Foundation.
PY - 1998
Y1 - 1998
N2 - Our earlier studies have shown development of endothelial dysfunction in the feline renal artery during hemorrhagic hypotension. Because L-arginine (L-Arg), the precursor of nitric oxide (NO), reportedly improves endothelial function in several pathophysiological states including hypotension, we investigated its possible beneficial effect on the adrenal and renal circulations during hemorrhagic hypotension in anesthetized, 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 hemodynamic effects in normotension but prevented the increase of the vascular resistance and improved blood flow in the adrenal cortex during hypotension. In the kidney, L-Arg also prevented hemorrhage-induced vasoconstriction, although its effect on blood flow did not reach significance. 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 resistances to a similar extent as that observed during hypotension. It thus seems that an L-Arg-reversible dysfunction of the endothelial NO-synthesizing pathway contributes to hemorrhage-induced adrenal and renal vasoconstriction.
AB - Our earlier studies have shown development of endothelial dysfunction in the feline renal artery during hemorrhagic hypotension. Because L-arginine (L-Arg), the precursor of nitric oxide (NO), reportedly improves endothelial function in several pathophysiological states including hypotension, we investigated its possible beneficial effect on the adrenal and renal circulations during hemorrhagic hypotension in anesthetized, 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 hemodynamic effects in normotension but prevented the increase of the vascular resistance and improved blood flow in the adrenal cortex during hypotension. In the kidney, L-Arg also prevented hemorrhage-induced vasoconstriction, although its effect on blood flow did not reach significance. 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 resistances to a similar extent as that observed during hypotension. It thus seems that an L-Arg-reversible dysfunction of the endothelial NO-synthesizing pathway contributes to hemorrhage-induced adrenal and renal vasoconstriction.
KW - Endothelium
KW - Hemorrhagic hypotension
KW - N(G)-nitro-L-arginine
KW - Nitric oxide
KW - Shock
KW - Vascular resistance
KW - Vasoconstriction
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U2 - 10.1046/j.1523-1755.1998.06754.x
DO - 10.1046/j.1523-1755.1998.06754.x
M3 - Article
C2 - 9736297
AN - SCOPUS:0031751828
SN - 0098-6577
VL - 54
SP - S221-S223
JO - Kidney International, Supplement
JF - Kidney International, Supplement
IS - 67
ER -