Nonnoradrenergic mechanism of reflex cutaneous vasoconstriction in men

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 α-adrenergic receptors, 2) Yoh plus propranolol (5 mM Yoh-1 mM PR id) to block α- and β-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 (T_SK) was controlled at 34°C (water-perfused suit) for 10 rain 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 T_SK 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.