Low levels (i.e., 20 mmHg) of lower body negative pressure (LBNP) have been utilized to unload "selectively" cardiopulmonary baroreceptors in humans, since steady-state mean arterial pressure and heart rate (HR) have been found unchanged at such levels. However, transient reductions in blood pressure (BP) followed by reflex compensation may occur without detection, which could unload arterial baroreceptors. The purposes of this study were to test the hypothesis that the arterial baroreflex is engaged even during low levels of LBNP and to determine the time course of changes in hemodynamics. Fourteen healthy individuals (age range 20 to 54) were studied. BP (Portapres & Suntech), HR (ECG), pulmonary capillary wedge pressure or pulmonary artery diastolic pressure, and right atrial pressure (PCWP or PDP, and RAP, Swan-Ganz catheter), and hemodynamics (Modelflow) were recorded continuously at baseline, -15 and -30 mmHg LBNP for 6 min each. Application of -15 mmHg LBNP resulted in rapid and sustained falls in RAP and PCWP or PDP, progressive decreases in cardiac output and stroke volume, followed subsequently by transient reductions in both systolic and diastolic BP which were then restored through the arterial baroreflex feedback mechanism after approximately 15 heart beats. Additional studies were performed in 5 subjects with pulmonary artery catheterization, and this transient reduction in BP was observed in three at -5 and in all at -10 mmHg LBNP. The delay for left ventricular stroke volume to fall at -15 mmHg LBNP was about 10 cardiac cycles. Steady-state BP and HR remained unchanged during mild LBNP; however, BP decreased while HR increased at -30 mmHg LBNP. These results suggest that arterial baroreceptors are consistently unloaded during low levels (i.e., -10 and -15 mmHg) of LBNP in humans. Thus, "selective" unloading of cardiopulmonary baroreceptors cannot be presumed to occur during these levels of mild LBNP.