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1 Department of Physiology, University of Texas Health Science Center, San Antonio, Texas, USA
* To whom correspondence should be addressed. E-mail: johnson{at}uthscsa.edu.
Previous work indicates that sympathetic nerves participate in the vascular responses to direct cooling of the skin in humans. We evaluated this hypothesis further in a four part series by measuring changes in cutaneous vascular conductance (CVC from forearm skin locally cooled from 34°C to 29°C for 30 minutes. In Part 1 bretylium tosylate reversed the initial vasoconstriction (-14 ±6.6% control CVC; first 5 minutes) to one of vasodilation (+19.7 ±7.7%), but did not affect the response at 30 minutes (-30.6 ±9% control, -38.9 ±6.9% bretylium; both p<0.05, p>0.05 between treatments). Part 2: Yohimbine and propranolol (YP) also reversed the initial vasoconstriction (-14.3 ±4.2% control) to vasodilation (+26.3 ±12.1% YP), without a significant effect on the 30 min response (-26.7 ±6.1% YP, -43.2 ±6.5% control; both p<0.05, p>0.05 between sites). Part 3: The NPY Y1 receptor antagonist BIBP 3226, had no significant effect on either phase of vasoconstriction (p>0.05 between sites both times). Part 4: Sensory nerve blockade by anesthetic cream (Emla) also reversed the initial vasoconstriction (-20.1 ±6.4% control) to one of vasodilation (+213.4 ±87.0% Emla), whereas the final levels did not differ significantly (-37.7 ±10.1% control, -37.2 ±8.7% Emla; both p<0.05, p>0.05 between treatments). These results indicate that local cooling causes cold sensitive afferents to activate sympathetic nerves to release norepinephrine, leading to a local cutaneous vasoconstriction that masks a non-neurogenic vasodilation. Later, a vasoconstriction develops with or without functional sensory or sympathetic nerves.
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