The present study evaluated the acute effects of angiotensin II (ANG II, 5 to 480 ng.kg^-1 iv) and phenylephrine (PHE, 0.2 to 146 ng.kg^-1 iv) on total renal (RBF) and medullary (MBF) blood flow in anesthetized Lyon hypertensive (LH) and low blood pressure (LL) rats. ANG II and PHE induced dose-dependent decreases in both RBF and MBF which were greater in LH than in LL rats. Interestingly, after ANG II, but not after PHE, the initial medullary vasoconstriction was followed by a long-lasting and dose-dependent vasodilation which was significantly blunted in LH compared to LL rats. The mechanisms of the MBF effects of ANG II were studied in LL rats only. Blockade of AT1 receptors with losartan (10 mg.kg^-1) abolished all the effects of ANG II while AT2 receptors blockade with PD 123319 (50 µg.kg^-1.min^-1 iv) did not change these effects. Indomethacin (5 mg.kg^-1) decreased by about 90% the medullary vasodilation induced by the lowest doses of ANG II (from 15 ng.kg^-1min^-1). In contrast, N^G-nitro-L-arginine methyl ester (L-NAME, 10 mg.kg^-1 and 0.1 mg.kg^-1min^-1, iv) and the bradykinin B2 receptor antagonist, HOE-140 (20 µg.kg^-1 and 10 µg.kg^-1,min^-1, iv) markedly lowered the medullary vasodilation for the highest doses of ANG II only. In conclusion, this study shows that LH rats exhibit an altered MBF response to ANG II compared to LL rats and indicates that the AT1 receptor-mediated medullary vasodilator response to low doses of ANG II is mainly due to the release of prostaglandins, while the dilator response to high doses of ANG II has additional nitric oxide- and kinin-dependent components.