Role of renal nerves and endogenous dopamine in amino acid-induced glomerular hyperfiltration.

The present study was performed to clarify whether urinary dopamine excretion (UDAV) and renal nerves are involved in the increase in glomerular filtration rate (GFR) induced by amino acid (AA) infusion. In thiopental-anesthetized rats, L-phenylalanine-free solutions of 10 AA (10%) either with (AATyr, n = 10) or without (AA0, n = 10) L-tyrosine (0.5%) were infused. Compared with baseline values, AATyr increased GFR from 0.83 +/- 0.05 to 1.00 +/- 0.04 ml.min-1.100 g-1 (P < 0.01) and UDAV almost fivefold from 5.81 +/- 0.46 to 28.1 +/- 7.4 pmol.min-1.100 g-1 (P < 0.01). In contrast, infusion of AAo increased GFR as did AATyr but did not significantly change UDAV. The DA2-receptor antagonist S(-)-sulpiride dose-dependently (0.5 to 15 micrograms.min-1.100 g-1) inhibited the GFR response to AA infusion but did not affect UDAV. In rats that had undergone chronic bilateral renal denervation (DNX), the AA-induced hyperfiltration was abolished completely, regardless of whether L-tyrosine was present. DNX did not affect basal UDAV, but the increase in UDAV in response to AATyr was attenuated compared with rats with innervated kidneys. Renal sodium excretion was increased almost twofold due to AA infusion and did not correlate with UDAV significantly. The data suggest 1) that urinary dopamine does not play a significant role in the regulation of kidney function, 2) that renal innervation is essential in the GFR response to systemic AA infusion, and 3) that a dopaminergic mechanism apart from tubular dopamine excretion is involved as well.