Dopamine (DA) produces a natriuretic/diuretic response in the kidney by mcnisms that are still not well understood. There is some ination that DA2 receptors may be involved in mating the effects of DA, but little is known regarding the nature of this receptor in the kidney. Autoraigaphic localation of [3Hspiperone, a DA2 anta t, i ed that high-density binding was r ic to inner meduilary ting ducts (IMCDs) Exogenous dopamine (DA) produces a natriuretic/diuretic response in a variety of species, including humans (1, 2). The natriuretic effects of DA are generally thought to be due to an increase in renal blood flow and glomerular filtration rate (1) but may include direct tubular effects since low doses of DA increase urine output and urinary sodium excretion without altering renal hemodynamics (3-5). Although the mechanism of action ofDA within the kidney is not resolved, the effects ofDA on the kidney are blocked by DA receptor antagonists (2, 6, 7). DA receptors have been classified in the central nervous system as D1 and D2 (8) and in the periphery as DA1 and DA2 (9). A great deal of evidence indicates that vascular and tubular DA1 receptors are involved in mediating the actions of DA on the kidney (6, 7). Further support for a tubular site ofaction for DA comes from autoradiographic localization of DA1 receptors in rat kidney, which indicates that the highest levels are found in the proximal tubules (10, 11).Much less is known regarding the role of DA2 receptors in mediating the renal responses to DA. Spiperone, a central nervous system D2 antagonist, blocks the DA-stimulated increase in renal blood flow and sodium excretion in isolated perfused rat kidney (4). Bromocriptine, a DA2 agonist, has been reported to increase renal blood flow and singlenephron glomerular filtration rate in the rat (12,13