This study characterizes the location and subtype of peptide YY (PYY) receptors in rat and rabbit kidney and the effect of PYY on renal function and renal hemodynamics in rats. Receptor autoradiography performed on kidney sections revealed a dense concentration of specific high-affinity binding sites [dissociation constant (K(d)) = 0.7 ± 0.1 nM] in the papilla of the rat, as well as cortical and papillary binding in the rabbit (papilla, K(d) = 1.6 ± 0.6 nM) and some medullary binding in both species. In the rat papilla, neuropeptide Y (NPY) and the Y1 agonist, [Leu31, Pro34]NPY competed with PYY for binding (K(d) = 1.1 ± 0.4 nM and 1.6 ± 0.5 nM, respectively), but NPY-(13-36) (Y2 agonist) and pancreatic polypeptide (PP, Y4 agonist) were without effect, demonstrating that the PYY receptor in the rat papilla is of the Y1 subtype. In the rabbit papilla, NPY and NPY-(13- 36) competed with PYY (K(d) = 0.5 ± 0.1 and 3.1 ± 0.6 nM, respectively), but [Leu31, Pro34]NPY and PP were without effect, evidence that the PYY receptor in the rabbit papilla is of the Y2 subtype. Infusion of PYY into rats (47 pmol · kg-1 · min-1) increased mean arterial pressure (103 ± 6 to 123 ± 8 mmHg) and decreased renal plasma flow (13 ± 1.8 to 8.4 ± 2.1 ml/min) but produced no significant change in glomerular filtration rate or sodium excretion. Injection of PYY or angiotensin II directly into the renal artery caused a dose-related vasoconstriction, which was less intense but of longer duration for PYY than for angiotensin II. These results show that receptors for PYY are widely distributed in the kidney and that exogenously administered PYY causes renal vasoconstriction and may influence renal sodium excretion.