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Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229-3900
We tested for a nonnoradrenergic mechanism of reflex
cutaneous vasoconstriction with whole body progressive cooling in seven men. Forearm sites (<1 cm2) were pretreated with:
1) yohimbine (Yoh; 5 mM id) to antagonize 
-adrenergic
receptors, 2) Yoh plus propranolol (5 mM Yoh-1 mM PR id) to
block - and 
-adrenergic receptors, 3) iontophoretic application of bretylium tosylate (BT) to block all sympathetic vasoconstrictor nerve effects, or 4) intradermal saline.
Skin blood flow was measured by laser Doppler flowmetry and arterial pressure by finger photoplethysmography; cutaneous vascular conductance (CVC) was indexed as the ratio of the two. Whole body skin temperature (TSK) was controlled at 34°C (water-perfused suit) for 10 min and then lowered to 31°C over 15 min. During cooling,
vasoconstriction was blocked at BT sites (P > 0.05).
CVC at saline sites fell significantly beginning at TSK of
33.4 ± 0.01°C (P <0.05). CVC at Yoh-PR sites was
significantly reduced beginning at TSK of 33.0 ± 0.01°C
(P < 0.05). After cooling, iontophoretic application
of norepinephrine (NE) confirmed blockade of adrenergic receptors by
Yoh-PR. Because the effects of NE were blocked at sites showing
significant reflex vasoconstriction, a nonnoradrenergic mechanism in
human skin is indicated, probably via a sympathetic cotransmitter.
skin blood flow; sympathetic nervous system; cold stress; yohimbine; propranolol; -adrenergic receptors; cotransmitter
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