Angiotensin II (AngII) causes salt-sensitive hypertension. It is unclear whether this is due to the inability to suppress AngII during increased salt intake or increased plasma AngII itself. To distinguish between these mechanisms, Sprague Dawley rats were instrumented with arterial and venous catheters for measurement of arterial pressure and infusion of drugs respectively. The sensitivity of arterial pressure to salt was measured in four groups with the following treatments; 1) saline control (CON; N=12), 2) angiotensin converting enzyme inhibitor enalapril to block endogenous AngII (Ang-LO; N=10), 3) enalapril + 5 ng/kg/min AngII to clamp plasma AngII at normal levels (Ang-NORM; N=10), 4) enalapril+ 20 ng/kg/min AngII to clamp AngII at high levels (Ang-HI; N=10). Rats ingested a 0.4% NaCl diet for 3 days followed by 11 days of a 4.0% NaCl diet. Arterial pressure on 0.4% NaCl was lower in Ang-LO (84 ± 2 mmHg) compared to CON (101±3 mmHg) and Ang-NORM (98±4 mmHg) groups whereas Ang-HI rats were hypertensive (145±4 mmHg). Salt-sensitivity was expressed as the change in arterial pressure/change in sodium intake on the last day of 4.0% NaCl. Salt-sensitivity (mmHg/mEq Na) was lowest in CON rats (0.0±0.1) and progressed from Ang-LO (0.8±0.2), Ang-NORM (1.5±0.5) to Ang-HI (3.5±0.5) rats. We conclude that the major determinant of salt-sensitivity of arterial pressure is the basal level of plasma AngII rather than the responsiveness of the renin-angiotensin system.