Role of renal nerves and endogenous dopamine in amino acid-induced glomerular hyperfiltration
Mühlbauer, B.; Spöhr, F.; Schmidt, R.; Osswald, H.
American Journal of Physiology 273(1 Pt 2): F144-F149
1997
ISSN/ISBN: 0002-9513 PMID: 9249602 Document Number: 477339
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 (AA-Tyr n = 10) or without (AA-O, n = 10) L-tyrosine (0.5%) were infused. Compared with baseline values, AA-Tyr increased GFR from 0.83 +- 0.05 to 1.00 +- 0.04 ml cntdot min-1 cntdot 100 g-1 (P lt 0.01) and UDAV almost fivefold from 5.81 +- 0.46 to 28.1 +- 7.4 pmol cntdot min-1 cntdot 100 g-1 (P lt 0.01). In contrast, infusion of AA-0 increased GFR as did AA-Tyr but did not significantly change U-DAV. The DA-2-receptor antagonist S(-)-sulpiride dose-dependently (0.5 to 15 mu-g cntdot min-1 cntdot 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 AA-Tyr 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.