Activation of renal dopamine-1 receptors decreases sodium transport. However, the spontaneously hypertensive rat retains sodium despite increased renal dopamine concentration. We tested the hypothesis that the abnormal sodium handling in spontaneously hypertensive rats (Okamoto-Aoki strain) is related to a decreased dopaminergic response by studying the effects of the intrarenal infusion of the dopamine-1 agonist SKF-38393 and the dopamine-1 antagonist SCH-23390 in hypertensive and in normotensive Wistar-Kyoto rats. Rats (9–16 weeks old) were studied with renal nerves intact under pentobarbital anesthesia (n= 5–6 in each group). Specificity of dopamine-1 effects of SKF-38393 was verified because its natriuretic effect was blocked in a dose-related manner by the dopamine-1 antagonist SCH-23390 (n= 5). Intrarenal arterial infusion of the dopamine-1 agonist SKF-38393 did not affect glomerular filtration rate but resulted in a dose-related natriuresis and diuresis in normotensive but not in hypertensive rats. Intrarenal arterial infusion of the dopamine-1 antagonist SCH-23390 alone induced an antinatriuresis, without affecting glomerular filtration rate, in normotensive but not in hypertensive rats. Addition of the dopamine-2 antagonist YM- 09151 to the dopamine-1 antagonist infusion did not enhance the effect of the dopamine-1 antagonist The lack of response to the dopamine-1 agonist or antagonist in hypertensive rats was not due to differences in renal dopamine-1 receptor density (U ± 0 J pmol/mg protein for spontaneously hypertensive rats, n=4; l±0.2 for Wistar-Kyoto rats, n=4) or affinity, distribution determined by autoradiography was also similar. The abnormal renal sodium handling in 9–16-week-old spontaneously hypertensive rats is in part due to decreased response distal to the dopamine-1 receptor.