Previous studies have 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 to 31.7 degrees C. In protocol 1, Ringer solution and the NPY receptor antagonist BIBP-3226 alone were delivered intradermally via microdialysis. In protocol 2, yohimbine plus propranolol (Yoh + Pro), Yoh + Pro in combination with BIBP-3226, and Ringer 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-3226-treated sites, CVC fell by 34.1% to 65.9 +/- 5.0% (P < 0.05; P < 0.05 between sites). In protocol 2, during body cooling, CVC at control sites fell by 32.6%, to 67.4 +/- 4.3% of baseline; at sites treated with Yoh + Pro, 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 + Yoh + Pro (P > 0.05; P < 0.05 vs. other sites). After cooling, exogenous norepinephrine induced vasoconstriction at control sites (P < 0.05) but not at sites treated with Yoh + Pro + BIBP-3226 (P > 0.05). These results indicate that NPY participates in sympathetically mediated cutaneous vasoconstriction in humans during whole body cooling.
Active vasodilatation (AVD) in human, non-glabrous skin depends on functional cholinergic fibres but not on acetylcholine (ACh). We tested whether AVD is a redundant system in which ACh and vasoactive intestinal polypeptide (VIP) are co-released from cholinergic nerves.
The distribution of the reflex effects of isometric exercise on cutaneous vasomotor and sudomotor function is not clear. We examined the effects of isometric exercise by different muscle masses on skin blood flow (SkBF) and sweat rate (SR) in nonglabrous skin and in glabrous skin. The latter contains arteriovenous anastomoses (AVAs), which cause large fluctuations in SkBF. SkBF was measured by laser-Doppler flowmetry (LDF) and reported as cutaneous vascular conductance (CVC; LDF/mean arterial pressure). SR was measured by capacitance hygrometry. LDF and SR were measured at the sole, palm, forearm, and ventral leg during separate bouts of isometric handgrip (IHG) and isometric leg extension (ILE). CVC and its standard deviation decreased significantly during IHG and ILE in the palm and sole (P < 0.05) but not in the forearm or leg (P > 0.05). Only palmar SR increased significantly during IHG and ILE (P < 0.05). We conclude that the major reflex influences of isometric exercise on the skin include AVAs and palmar sweat glands and that this is true for both arm and leg exercise.
We tested whether a nonnoradrenergic component of reflex vasoconstriction of skin blood flow (SkBF) is sensitive to female reproductive hormones. Six women taking oral contraceptives underwent whole-body cooling during high-hormone (HH) and low-hormone (LH) phases of oral contraceptive use. SkBF was monitored by laser Doppler flowmetry (LDF) at sites treated by intradermal injection of yohimbine-propranolol (5 mM and 1 mM; YOPR) to block the effects of norepinephrine (NE) or at saline (Sal) control sites. Mean arterial pressure (MAP) was measured with the use of the Penaz method. Cutaneous vascular conductance (CVC = LDF/mean arterial pressure) was expressed as a percentage of baseline. Whole body skin temperature was decreased from 34 to 31 degrees C in HH and LH. In both HH and LH, CVC at Sal-treated sites was reduced during cooling (CVC = 53.1 +/- 8.6% and 54.4 +/- 4.2%, both P < 0.05). In HH, CVC at YOPR sites was reduced during cooling (78.8 +/- 3.6%, P < 0.05). In contrast, CVC at YOPR sites was not reduced significantly during cooling in LH (CVC = 95.9 +/- 2.8%, P > 0.05). Across phases, CVC at YOPR sites during cooling was significantly different (P < 0.05). After cooling, the effects of NE at YOPR sites were completely blocked. These data indicate that a nonnoradrenergic mechanism of reflex cutaneous vasoconstriction is present in women and is associated with reproductive hormone status.
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