Background/Aims: Angiotensin II (ANG II) and dopamine (DA) are both important regulators of sodium and water transport across renal proximal tubules. Previous studies demonstrate that atrial natriuretic factor (ANF) can regulate renal DA uptake and thereby Na<sup>+</sup>,K<sup>+</sup>-ATPase activity in the external renal cortex. As ANG II counteracts most of the ANF biological effects, the aim of the present study was to evaluate ANG II effects on renal DA metabolism and identify the receptor involved. Methods: To determine ANG II effects on renal DA metabolism, we evaluated <sup>3</sup>H-DA uptake in vitro in kidney tissue samples from Sprague-Dawley rats. Results: The results indicate that ANG II decreased DA uptake at 30 min, in a concentration-response fashion, in the external and juxtamedullar cortex. DA uptake was characterized as an extraneuronal uptake and decreased at 0°C and in sodium-free medium. The biological receptor type involved was AT<sub>1</sub>, since losartan reversed ANG II effects on DA uptake while AT<sub>2</sub> receptors were not involved since PD 123319 did not affect ANG II effects. The absence of sodium did not alter the ANG II response. Conclusion: ANG II inhibits DA uptake by kidney tubular cells. These effects implicate AT<sub>1</sub> receptors without participation of AT<sub>2</sub> receptors. This mechanism could be related to the DA effects on sodium reabsorption and linked to ANG II antinatriuretic effects in the kidney.