The CO2 reactivity was calculated at mean arterial blood pressure (MABP) values ranging from 40 to 140 mm Hg in 15 normotensive volunteers and in 7 patients with chronic arterial hypertension. The cerebral vascular reactivity (CVR) was estimated from indirect measurements of cerebral blood flow (CBF) by the arteriovenous oxygen saturation method. In all subjects but one of the hypertensive patients, there was a significant linear correlation of CVR with PaCO2 over the total range of MABP. The median CO2 reactivity in the volunteers and in the hypertensive patients was 2.7 and 2.8% CBF/0.1 kPa, respectively (NS). At MABP values corresponding to the plateau of CBF autoregulation (baseline MABP +/- 20%), the median CO2 reactivity was 3.0% CBF/0.1 kPa in both groups. During a cross-sectional correlation analysis of the pooled data from all volunteers, the CO2 reactivity increased with increasing MABP in the range of 50-110 mm Hg. Outside this range there was no correlation of CVR with PaCO2. In conclusion, our results confirmed that during acute hypo- and hypertension, the influence of PaCO2 on the CVR is reduced. The full CO2 reactivity of the cerebral vessel exists only at the plateau of CBF autoregulation.