The present study was conducted to test the hypothesis that salt dependent hypertension, in rats with an unresponsive renin-angiotensin system, is characterized by a "whole body autoregulation" hemodynamic profile. To test this hypothesis, rats were chronically instrumented to continuously measure cardiac output (CO) and arterial pressure (AP). A venous catheter was implanted for infusion of saline vehicle (Veh; n=8), or treatment [enalapril (2 mg/kg/day) plus angiotensin II (AngII): (Ang-NORM; 5 ng/kg/min, n=8), or (Ang-HI; 10 ng/kg/min, n=9)] to pharmacologically clamp plasma AngII. After a 10-day recovery period on 0.1% NaCl diet, AP and CO was measured continuously for 5 days of control (0.1% NaCl), 7 days of high salt (4.0% NaCl), and 5 days of recovery (0.1% NaCl). Hemodynamics did not change in the Veh group at any time. AP increased by ~20 mmHg in the Ang-NORM and Ang-HI groups when NaCl was increased. Hypertension was mediated by an increase in CO of ~12% at steady state, with no change in TPR during the high salt period. AP returned to control levels when dietary sodium was decreased, mediated by a ~10% decrease in TPR, with CO remaining elevated. There was no difference in the hemodynamic responses to increased salt between the Ang-HI and Ang-NORM groups. We conclude that the whole body autoregulation hypothesis does not explain the hemodynamic profile of salt dependent hypertension in rats with an unresponsive renin angiotensin system.