RT Journal Article SR Electronic T1 Dopamine D2 Receptors Mediate Glomerular Hyperfiltration Due To Amino Acids JF Journal of Pharmacology and Experimental Therapeutics JO J Pharmacol Exp Ther FD American Society for Pharmacology and Experimental Therapeutics SP 1248 OP 1252 VO 286 IS 3 A1 Gerd Luippold A1 Bernd Mühlbauer YR 1998 UL http://jpet.aspetjournals.org/content/286/3/1248.abstract AB 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. The American Society for Pharmacology and Experimental Therapeutics