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1 Department of Exercise and Movement Science, University of Oregon, Eugene, OR, USA
2 Oregon Heart Center, Sacred Heart Medical Center, Eugene, OR, USA
3 Noll Physiological Research Center, The Pennsylvania State University, University Park, PA, USA
* To whom correspondence should be addressed. E-mail: lalex{at}gladstone.uoregon.edu.
Thermoregulatory cutaneous vasodilation is diminished in the elderly. The goal of this study was to test the hypothesis that a reduction in NO-dependent mechanisms contributes to the attenuated reflex cutaneous vasodilation in older subjects. Seven young (23±2) and seven older (71±6) men were instrumented with two microdialysis fibers in the forearm skin. One site served as control (Ringer's infusion) and the second site was perfused with 10mM L-NAME to inhibit NO-synthase (NOS) throughout the protocol. Water-perfused suits were used to raise core temperature 1.0oC. Skin blood flow was measured using laser-Doppler flowmetry (LDF) over each microdialysis fiber. Cutaneous vascular conductance (CVC) was calculated as LDF/MAP, with values expressed as a percentage of maximal vasodilation (infusion of 28mM sodium nitroprusside). NOS inhibition reduced CVC from 75±6% CVCmax to 53±3% CVCmax in the young and from 64±5% CVCmax to 29±2% CVCmax in the older subjects with a 1.0oC rise in core temperature. Thus, the relative NO-dependent portion of cutaneous active vasodilation (AVD) accounted for approximately 23% of vasodilation in the young and 60% of the vasodilation in the older subjects at this level of hyperthermia (p<0.001). In summary, NO-mediated pathways contributed more to the total vasodilatory response of the older subjects at high core temperatures. This suggests attenuated cutaneous vasodilation with age may be due to a reduction in, or decreased vascular responsiveness to, the unknown neurotransmitter(s) mediating AVD.
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