Sympathetic regulation of the human cerebrovascular response to carbon dioxide

Peebles KC, Ball OG, MacRae BA, Horsman HM, Tzeng YC. Sympathetic regulation of the human cerebrovascular response to carbon dioxide. J Appl Physiol 113: 700-706, 2012. First published June 28, 2012; doi: 10.1152/japplphysiol.00614.2012.-Although the cerebrovasculature is known to be exquisitely sensitive to CO2, there is no consensus on whether the sympathetic nervous system plays a role in regulating cerebrovascular responses to changes in arterial CO2. To address this question, we investigated human cerebrovascular CO2 reactivity in healthy participants randomly assigned to the alpha(1)-adrenoreceptor blockade group (9 participants; oral prazosin, 0.05 mg/kg) or the placebo control (9 participants) group. We recorded mean arterial blood pressure (MAP), heart rate (HR), mean middle cerebral artery flow velocity (MCAV mean), and partial pressure of end-tidal CO2 (PETCO2) during 5% CO2 inhalation and voluntary hyperventilation. CO2 reactivity was quantified as the slope of the linear relationship between breath-to-breath PETCO2 and the average MCAv(mean) within successive breathes after accounting for MAP as a covariate. Prazosin did not alter resting HR, PETCO2, MAP, or MCAV mean. The reduction in hypocapnic CO2 reactivity following prazosin (-0.48 +/- 0.093 cm.s(-1).mmHg(-1)) was greater compared with placebo (-0.19 +/- 0.087 cm.s(-1).mmHg(-1); P < 0.05 for interaction). In contrast, the change in hypercapnic CO2 reactivity following prazosin (-0.23 cm.s(-1).mmHg(-1)) was similar to placebo (-0.31 cm.s(-1).mmHg(-1); P = 0.50 for interaction). These data indicate that the sympathetic nervous system contributes to CO2 reactivity via alpha(1)-adrenoreceptors; blocking this pathway with prazosin reduces CO2 reactivity to hypocapnia but not hypercapnia.