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2C-adrenergic receptors enable
cold-induced vasoconstriction in cutaneous arteries
1 Heart and Lung Institute, Ohio State University, Columbus, Ohio 43210; and 2 Department of Comparative Medicine, Stanford University, Stanford, California 94305
Cold constricts cutaneous blood vessels by increasing the
reactivity of smooth muscle 
2-adrenergic receptors
(2-ARs). Experiments were performed to determine the
role of 2-AR subtypes (2A-, 2B-, 2C-ARs) in this response.
Stimulation of 1-ARs by phenylephrine or
2-ARs by UK-14,304 caused constriction of isolated mouse
tail arteries mounted in a pressurized myograph system. Compared with proximal arteries, distal arteries were more responsive to
2-AR activation but less responsive to activation of
1-ARs. Cold augmented constriction to
2-AR activation in distal arteries but did not affect
the response to 1-AR stimulation or the level of
myogenic tone. Western blot analysis demonstrated expression of
2A- and 2C-ARs in tail arteries:
expression of 2C-ARs decreased in distal compared with
proximal arteries, whereas expression of the glycosylated form of the
2A-AR increased in distal arteries. At 37°C,
2-AR-induced vasoconstriction in distal arteries was
inhibited by selective blockade of 2A-ARs (BRL-44408)
but not by selective inhibition of 2B-ARs (ARC-239) or
2C-ARs (MK-912). In contrast, during cold exposure
(28°C), the augmented response to UK-14,304 was inhibited by the
2C-AR antagonist MK-912, which selectively abolished cold-induced amplification of the response. These experiments indicate
that cold-induced amplification of 2-ARs is mediated by
2C-ARs that are normally silent in these cutaneous
arteries. Blockade of 2C-ARs may prove an effective
treatment for Raynaud's Phenomenon.
Raynaud's Phenomenon; scleroderma; microcirculation; thermoregulation; vascular smooth muscle
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