Recent evidence suggests that elevated sodium levels may exacerbate the hypertensive effects of AngII by acting at sodium sensing neurons in certain circumventricular organs of the brain. The purpose of this study was to examine the AP’s role in AngII-induced hypertension during periods of normal and elevated dietary salt. We hypothesized that an intact AP was necessary for the full development of hypertension under chronic AngII infusion and that its role would be pronounced during periods of increased dietary sodium. To test this, male Sprague-Dawley rats underwent area postrema lesion (APx, n=6) or sham operation (sham, n=6) and were instrumented with radio-telemetry transducers and venous catheters. After a 3 day control period of 0.9% saline infusion (7 ml/day) and 0.4% dietary sodium, rats received a 10 day infusion of AngII (10 ng/kg/min) followed by a second 10 day infusion during which rats were fed a 4.0% sodium diet. By day 6 of AngII infusion, mean arterial pressure (MAP) in APx rats had increased to 139 ± 4 mmHg while MAP in sham rats had increased to 126 ± 3 mmHg. This difference was found to be significant and continued through day 1 of the high salt period. On day 8 of high salt, MAP was again observed to be significantly higher (162 ± 1 mmHg) in APx rats when compared to sham rats (147 ± 4 mmHg.) These results do not support the hypothesis that the AP is necessary for the full development of AngII-induced hypertension at normal or elevated levels of dietary sodium.