DOPAMINE D-2 RECEPTORS MEDIATE GLOMERULAR HYPERFILTRATION DUE TO AMINO-ACIDS

Renal dopamine has been proposed to be involved in the regulation of g lomerular filtration rate (GFR). Because inhibition of dopamine D-2 re ceptors abolishes the renal hyperfiltration due to amino acid load, we tested the hypothesis that pharmacological activation of D-2-like rec eptors mimicked this renal response. In anesthetized rats, quinpirole (0.3 mu g . 100 g(-1 .) min(-1)), an agonist for receptors of the D-2- like family, caused an increase in GFR by 20 +/- 2%, which corresponde d to that provoked by infusion of an 10% amino acid solution. The D-2 receptor antagonist S(-)-sulpiride that acts both centrally and periph erally completely abolished the renal hemodynamic response to quinpiro le and to amino acids whereas domperidone, a peripherally acting D-2 r eceptor antagonist, inhibited this hyperfiltration only in part. Urina ry dopamine excretion increased in response to amino acid infusion whe ther GFR increased or not. We conclude that, in anesthetized rats, dop amine D-2 receptors contribute to the amino acid-induced hyperfiltrati on and that both central and peripheral receptors might be involved, w hereas dopamine excreted into the urine does not appear to play a func tional role in this renal hemodynamic response.