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J Appl Physiol 88: 467-472, 2000;
8750-7587/00 $5.00
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Vol. 88, Issue 2, 467-472, February 2000

Effects of atropine and L-NAME on cutaneous blood flow during body heating in humans

Shubha Shastry1, Christopher T. Minson2, Shurea A. Wilson2, Niki M. Dietz2, and Michael J. Joyner2

Departments of 1 Physiology and Biophysics and 2 Anesthesiology, Mayo Clinic and Foundation, Rochester, Minnesota 55905

We sought to investigate further the roles of sweating, ACh spillover, and nitric oxide (NO) in the neurally mediated cutaneous vasodilation during body heating in humans. Six subjects were heated with a water-perfused suit while cutaneous blood flow was measured with a laser-Doppler flowmeter. After a rise in core temperature (1.0 ± 0.1°C) and the establishment of cutaneous vasodilation, atropine and subsequently the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) were given to the forearm via a brachial artery catheter. After atropine infusion, cutaneous vascular conductance (CVC) remained constant in five of six subjects, whereas L-NAME administration blunted the rise in CVC in three of six subjects. A subsequent set of studies using intradermal microdialysis probes to selectively deliver drugs into forearm skin confirmed that atropine did not affect CVC. However, perfusion of L-NAME resulted in a significant decrease in CVC (37 ± 4%, P < 0.05). The results indicate that neither sweating nor NO release via muscarinic receptor activation is essential to sustain cutaneous dilation during heating in humans.

nitric oxide; sudomotor; muscarinic


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