Role of endothelium-derived nitric oxide in the renal hemodynamic response to amino acid infusion

The present study was performed in anesthetized rats to compare the renal hemodynamic responses to mixed amino acids (M-AA) with those to L-arginine (L-Arg) and to examine the effect of endothelium-derived nitric oxide (EDNO) synthesis blockade on the M-AA-induced rise in renal plasma flow (RPF) and glomerular filtration rate (GFR). Intravenous infusion of both M-AA (Ser, Gly, Ala, and Pro, 0.71 mmol · 100 g^-1 · min^-1) and L-Arg (0.71 mmol · 100 g^-1 · min^-1) increased RPF and GFR. Peak increases in RPF for M-AA and L-Arg were 39.7% (P < 0.05) and 63.4% (P < 0.01), whereas GFR increases were 33.6% (P < 0.05) and 46.7% (P < 0.01, respectively). Outer cortical blood flow (OCBF) was increased with both treatments. Sodium excretion and urine flow were increased more with L-Arg than M-AA (both P < 0.01). Infusion of the nitric oxide synthesis inhibitor, nitro-L-arginine (N-L-Arg, 20 μg · 100 g^-1 · min^-1) increased mean arterial pressure but decreased RPF 48.4% (P < 0.001), OCBF 39.5% (P < 0.001), GFR 37.8% (P < 0.01), urine flow 29.8% (P < 0.01), and sodium excretion 40.9% (P < 0.01). When M-AA was administered after N-L-Arg, significant increases in OCBF, RPF, and GFR were observed (P < 0.01); there was also an enhancement of sodium excretion and urine flow (both P < 0.05). In addition, during co-infusion of M-AA and N-L- Arg, renal hemodynamics and excretory function values were significantly greater than those obtained during N-L-Arg alone. These results provide further evidence that EDNO alters the baseline level of renal hemodynamics. However, the enhancement of OCBF, RPF, GFR, urine flow, and sodium excretion by M-AA during EDNO blockade suggests that mechanisms in addition to EDNO contribute to the renal responses to amino acid infusion.