Baroreflex-induced sympathetic activation does not alter cerebrovascular CO2 responsiveness in humans

We investigated the effect of baroreflex-induced sympathetic activation, produced by lower body negative pressure (LBNP) at -40 mmHg, on cerebrovascular responsiveness to hyper- and hypocapnia in healthy humans. Transcranial Doppler ultrasound was used to measure blood flow velocity (CFV) in the middle cerebral artery during variations in end-tidal carbon dioxide pressure (PIT,11,)of +10, +5,0,-5, and -10 mmHg relative to eupnoea. The slopes of the linear relationships between PET,CO, and CFV were computed separately for hyper- and hypocapnia during the LBNP and no-LBNP conditions. LBNP decreased pulse pressure, but did not change mean arterial pressure. LBNP evoked an increase in ventilation that resulted in a 9 2 mmHg decrease in P-ET,P-CO2, which was corrected by CO2 supplementation of the inspired air. LBNP did not affect cerebrovascular CO2 response slopes during steady-state hypercapnia (3.14 +/- 0.24 vs. 2.96 +/- 0.26 cm s(-1) mmHg(-1)) or hypocapnia (1.31 +/- 0.18 vs. 1.32 +/- 0.19 cm s(-1) mmHg(-1)), or the CFV responses to voluntary apnoea (+51 +/- 19 vs. +50 +/- 18 %). Thus, cerebrovascular CO2 responsiveness was not altered by baroreflex-induced sympathetic activation. Our data challenge the concept that sympathetic activation restrains cerebrovascular responses to alterations in CO2 pressure.