There is evidence that alterations in heart rate and blood pressure variability (BPV) are associated with cardiovascular disease. We used a mice model to investigate the effects of acute and chronic stress on blood pressure variability (BPV) and heat rate variability (HRV). Shaker stress was given acutely (5 min, 150 cycles/min) and chronically (3 days, 2 min stress, 150 cycles/min, 45 sessions/day) in male C57BLJ mice. Systolic arterial pressure (SAP) and pulse interval (PI) time series were submitted to autoregressive spectral analysis with variability measured in the low-frequency (LF, 0.1-1.0 Hz) and high-frequency (HF, 1-5 Hz) ranges. In the acute experiment, MAP was increased significantly in the first 10 min poststress period (99+/-2 vs. 113+/-2 mm Hg) and returned to control levels 30 min poststress. HR was significantly higher in the initial poststress period (537+/-12 vs. 615+/-20 bpm). These alterations were associated with a marked increase in BPV (21+/-4 vs. 55+/-11 mm Hg2) and in power of LF oscillations (18+/-3 vs. 42+/-7 mm Hg2). On the other hand, chronic stress exposure produced a reduction in BPV (16+/-4 vs. 6+/-1 mm Hg2) and LF oscillations (11+/-3 vs. 3+/-1 mm Hg2). HRV was not altered after either acute or chronic stress. Spontaneous baroreflex sensitivity (SBS), determined by cross-spectral analysis between PI and BP, was reduced significantly in acute stress (-50%), but unchanged in chronic stress. Our results show that acute stress produced changes in BPV that may be associated with increased sympathetic activity and a reduction in blood pressure buffering. Under chronic conditions, there is no alteration in baroreflex sensitivity while BPV is reduced. This is likely related to the combination of sympathetic activation in the face of vasculature alterations.