Abstract

Renal dopamine has been proposed to be involved in the regulation of glomerular filtration rate (GFR). Because inhibition of dopamine D₂ receptors abolishes the renal hyperfiltration due to amino acid load, we tested the hypothesis that pharmacological activation of D₂-like receptors mimicked this renal response. In anesthetized rats, quinpirole (0.3 μg · 100 g⁻¹ · min⁻¹), an agonist for receptors of the D₂-like family, caused an increase in GFR by 20 ± 2%, which corresponded to that provoked by infusion of an 10% amino acid solution. The D₂ receptor antagonist S(−)-sulpiride that acts both centrally and peripherally completely abolished the renal hemodynamic response to quinpirole and to amino acids whereas domperidone, a peripherally acting D₂receptor antagonist, inhibited this hyperfiltration only in part. Urinary dopamine excretion increased in response to amino acid infusion whether GFR increased or not. We conclude that, in anesthetized rats, dopamine D₂ receptors contribute to the amino acid-induced hyperfiltration and that both central and peripheral receptors might be involved, whereas dopamine excreted into the urine does not appear to play a functional role in this renal hemodynamic response.