Angiotensin II (AngII) can cause significant decreases in renal blood flow, but the sustained effect on renal blood flow and the relationship to the hypertensive response to AngII are not known. This study measured that relationship by infusing AngII (sc.) via osmotic minipump in C57BL/6 mice instrumented either with chronic renal artery flow probes or with DSI arterial pressure telemetry devices. All mice were fed a high salt diet (4% NaCl) throughout the study, and they were allowed at least one week of recovery from surgery before control measurements. Mice in the 90 ng/min mean arterial pressure (MAP) group (n=4) had a baseline MAP of 115±2 mmHg, and AngII infusion increased MAP to 158±3 mmHg. The 90 ng/min renal blood flow (RBF) mice (n=4) had a rapid decrease in RBF (measured 4 hrs/day) that was sustained for the 7‐day period, averaging 45.2±11.9 % of control. RBF returned rapidly to control levels during the recovery period. In the 20 ng/min mice, AngII increased MAP from 118±3 to 152±3 mmHg (n=3), and the RBF response (n=2) was the same as in the 90 ng/min mice. A “slow‐pressor” dose of AngII (6 ng/min, n=3) did not change RBF over a 14‐day infusion period. These results show that maximal hypertensive doses of AngII cause marked and sustained decreases in RBF, but that slower‐developing hypertension may not be linked to a renal vasoconstrictor mechanism. (AHA SDG ABB, HL 56259, HL 74167 MWB).