We sought to investigate further the roles of sweating, ACh spillover, and
nitric oxide (NO) in the neurally mediated cutaneous vasodilation during bo
dy heating in humans. Six subjects were heated with a water-perfused suit w
hile cutaneous blood flow was measured with a laser-Doppler flowmeter. Afte
r a rise in core temperature (1.0 +/- 0.1 degrees C) and the establishment
of cutaneous vasodilation, atropine and subsequently the NO synthase inhibi
tor N-G-nitro-L-arginine methyl ester (L-NAME) were given to the forearm vi
a a brachial artery catheter. After atropine infusion, cutaneous vascular c
onductance (CVC) remained constant in five of six subjects, whereas L-NAME
administration blunted the rise in CVC in three of six subjects. A subseque
nt set of studies using intradermal microdialysis probes to selectively del
iver drugs into forearm skin confirmed that atropine did not affect CVC. Ho
wever, 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 dilati
on during heating in humans.