New evidence for baroreflex and respiratory chemoreflex-mediated cerebral sympathetic activation in humans.

Abstract

The brain is highly innervated by sympathetic nerve fibers; however, their physiological purpose is poorly understood. We hypothesized that unilateral cerebral norepinephrine (NE) spillover, an index of cerebral sympathetic nerve activity (SNA), would be elevated when engaging the baroreflex [via lower-body negative pressure (LBNP; -20 and -40 Torr)] and respiratory chemoreflexes [via carbon dioxide (CO₂) administration (+8 Torr)], independently and in combination. Twelve young and healthy participants (five females) underwent simultaneous blood sampling from the right radial artery and internal jugular vein. Tritiated NE was infused through the participants' right forearm vein. Right internal jugular vein and internal carotid artery blood flow were measured using duplex ultrasound. Unilateral cerebral NE spillover remained unchanged when only LBNP was applied (P = 0.29) but increased with hypercapnia (P = 0.035) and -40 Torr LBNP + CO₂ (P < 0.01). There were no changes in total NE spillover during the LBNP and LBNP + CO₂ trials (both P = 0.66), nor during CO₂ alone (P = 0.13). No correlations were present between the increase in unilateral cerebral NE spillover during -40 Torr LBNP + CO₂ and reductions in internal carotid artery blood flow (P = 0.56). These results indicate that baroreflex and respiratory chemoreflex stressors elevate cerebral SNA; however, the observed cerebral sympathetic activation has no impact on blood flow regulation in the internal carotid artery.NEW & NOTEWORTHY The results of the current study suggest that baroreflex and respiratory chemoreflex stressors elevate cerebral sympathetic nervous activity, quantified using the brain norepinephrine spillover method. However, the observed cerebral sympathetic activation has no impact on blood flow regulation in the internal carotid artery.