title: Sympathetic regulation of the human cerebrovascular response to carbon dioxide.
abstract: Although the cerebrovasculature is known to be exquisitely sensitive to CO(2), there is no consensus on whether the sympathetic nervous system plays a role in regulating cerebrovascular responses to changes in arterial CO(2). To address this question, we investigated human cerebrovascular CO(2) reactivity in healthy participants randomly assigned to the α(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 (MCA(V mean)), and partial pressure of end-tidal CO(2) (Pet(CO(2))) during 5% CO(2) inhalation and voluntary hyperventilation. CO(2) reactivity was quantified as the slope of the linear relationship between breath-to-breath Pet(CO(2)) and the average MCAv(mean) within successive breathes after accounting for MAP as a covariate. Prazosin did not alter resting HR, Pet(CO(2)), MAP, or MCA(V mean). The reduction in hypocapnic CO(2) 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 CO(2) 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 CO(2) reactivity via α(1)-adrenoreceptors; blocking this pathway with prazosin reduces CO(2) reactivity to hypocapnia but not hypercapnia.
authors: Cardiovascular Systems Laboratory, Department of Surgery and Anaesthesia, University of Otago, Wellington South, New Zealand.
authors: K C
authors: KC
authors: Peebles
authors: O G
authors: OG
authors: Ball
authors: B A
authors: BA
authors: MacRae
authors: H M
authors: HM
authors: Horsman
authors: Y C
authors: YC
authors: Tzeng
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000328:Adult; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002245:Carbon Dioxide / Q000008:administration & dosage / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D006935:Hypercapnia / Q000139:chemically induced / Q000503:physiopathology; D016857:Hypocapnia / Q000503:physiopathology / Q000517:prevention & control; D008297:Male; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D055815:Young Adult
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D018340:Receptors, Adrenergic, alpha-1; D002245:Carbon Dioxide