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. 2008 Feb 29;138(1-2):114-7.
doi: 10.1016/j.autneu.2007.11.002. Epub 2007 Dec 4.

Diminished baroreflex-induced vasoconstriction following alpha-2 adrenergic receptor blockade in humans

D Walter Wray  1 , Peter B Raven, Mikael Sander
Affiliations

Diminished baroreflex-induced vasoconstriction following alpha-2 adrenergic receptor blockade in humans

D Walter Wray et al. Auton Neurosci. .

Abstract

The relative contribution of alpha adrenergic receptor subtypes in the transduction of sympathetic nerve activity (SNA) during carotid baroreflex (CBR) engagement is not well understood. Therefore, we compared the hemodynamic consequence of CBR-mediated sympatho-excitation via neck pressure (NP) before and after alpha-2 adrenergic blockade with intra-arterial yohimbine. Leg blood flow was measured using 2D and Doppler ultrasound, and arterial blood pressure was determined directly. NP caused the expected vasoconstriction, and this response was significantly reduced (by 50-60%) when NP was repeated after yohimbine. These data indicate that alpha-2 adrenergic receptors contribute significantly to CBR-induced vasoconstriction in the human leg under resting conditions.

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Figures

FIGURE 1
FIGURE 1
Leg blood flow (top panel) and vascular conductance (bottom panel) in response to sympatho-excitation from 5-sec neck pressure (NP). PRE, prior to NP. * Significantly different than PRE, P<0.05; § significantly different than control, P<0.05.
FIGURE 2
FIGURE 2
Relative changes in leg blood flow (left) and vascular conductance (right) in response to sympatho-excitation from 5-sec neck pressure (NP). YOH, yohimbine. § Significantly different than control, P<0.05.
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