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1 Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
* To whom correspondence should be addressed. E-mail: johnson{at}uthscsa.edu.
Previous studies provided evidence of a non-noradrenergic contributor to reflex cutaneous vasoconstriction in humans but did not identify the transmitter responsible. To test whether neuropeptide Y (NPY) has a role, in two series of experiments we slowly reduced whole-body skin temperature (TSK) from 34.5°C to 31.7°C. In Protocol 1 Ringers solution and the NPY receptor antagonist BIBP-3226 alone were delivered intradermally via microdialysis. In Protocol 2, yohimbine plus propranolol (YoPr), YoPr in combination with BIBP-3226, and Ringers solution were delivered to antagonize locally the vasomotor effects of NPY and norepinephrine. Blood flow was measured by laser Doppler flowmetry (LDF). Mean arterial blood pressure (MAP) was monitored at the finger (Finapres). In Protocol 1, cutaneous vascular conductance (CVC) fell by 45%, to 55.1±5.6% of baseline at control sites (p<0.05). At BIBP treated sites CVC fell by 34.1% to 65.9±5.0% (p<0.05, p<0.05 between sites). Protocol 2: during body cooling, CVC at control sites fell by 32.6%, to 67.4±4.3% of baseline; at sites treated with YoPr CVC fell by 18.7%, to 81.3±4.4% of baseline (p<0.05 vs. baseline; p<0.05 vs. control) and did not fall significantly at sites treated with BIBP-3226 plus YoPr (p>0.05; p<0.05 vs. other sites). Following cooling, exogenous norepinephrine induced vasoconstriction at control sites (P<0.05) but not at sites treated with YoPr plus BIBP-3226 (P>0.05). These results indicate that NPY participates in sympathetically mediated cutaneous vasoconstriction in humans during whole-body cooling.
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