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Articles in PresS, published online ahead of print August 30, 2002
J Appl Physiol, 10.1152/jap.00036.2002
Submitted on January 16, 2002
Accepted on August 21, 2002
1 Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, TX, USA; Faculty of Human Life and Environment, Nara Women's University, Nara, Japan
2 Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, TX, USA
3 Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, TX, USA; Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA
* To whom correspondence should be addressed. E-mail: craig.crandall{at}UTSouthwestern.edu.
Nitric oxide (NO) contributes to active cutaneous vasodilation during a heat stress in humans. Given that acetylcholine is released from cholinergic nerves during whole-body heating, coupled with evidence that acetylcholine causes vasodilation via NO mechanisms, it is possible that release of acetylcholine in the dermal space contributes to cutaneous vasodilation during a heat stress. To test this hypothesis, in seven subjects skin blood flow (SkBF) and sweat rate were simultaneously monitored over three microdialysis membranes placed in the dermal space of dorsal forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine (10 µM), the second membrane was perfused with the NO synthase inhibitor NG-nitro-L-arginine methyl ester (10 mM) dissolved in the aforementioned neostigmine solution (L-NAMENEO), while the third membrane was perfused with Ringer's solution as a control site. Each subject was exposed to approximately 20 min of whole-body heating via a water-perfused suit, which increased mean body temperature from 36.4±0.1 to 37.5±0.1 °C (P<0.05). After the heat stress SkBF at each site was normalized to its maximum value, identified by administration of 28 mM sodium nitroprusside. Mean body temperature threshold for cutaneous vasodilation was significantly lower at the neostigmine treated site relative to the other sites (neostigmine: 36.6±0.1 °C, L-NAMENEO: 37.1±0.1 °C, control: 36.9±0.1 °C), while no significant threshold difference was observed between the L-NAMENEO and control sites. At the end of the heat stress SkBF was not different between the neostigmine treated and control sites, while SkBF at the L-NAMENEO treated site was significantly lower than the other sites. These results suggest that acetylcholine released from cholinergic nerves is capable of modulating cutaneous vasodilation via NO synthase mechanisms early in the heat stress but not after substantial cutaneous vasodilation.
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