Sympathetic regulation of the human cerebrovascular response to carbon dioxide

• Published in: Journal of applied physiology (1985) Vol. 113; no. 5; pp. 700 - 706
• Main Authors: Peebles, K C, Ball, O G, MacRae, B A, Horsman, H M, Tzeng, Y C
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.09.2012
• Subjects: Adrenergic alpha-1 Receptor Antagonists - pharmacology; Adrenergic alpha-1 Receptor Antagonists - therapeutic use; Adult; Blood Flow Velocity - drug effects; Blood Flow Velocity - physiology; Blood pressure; Blood Pressure - drug effects; Blood Pressure - physiology; Carbon dioxide; Carbon Dioxide - administration & dosage; Carbon Dioxide - physiology; Cerebrovascular Circulation - drug effects; Cerebrovascular Circulation - physiology; Female; Heart rate; Heart Rate - drug effects; Heart Rate - physiology; Humans; Hypercapnia - chemically induced; Hypercapnia - physiopathology; Hypocapnia - physiopathology; Hypocapnia - prevention & control; Male; Nervous system; Receptors, Adrenergic, alpha-1 - physiology; Sympathetic Nervous System - drug effects; Sympathetic Nervous System - physiology; Veins & arteries; Young Adult
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00614.2012

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.