Role of nitric oxide synthase in human sweat gland output.

The mechanism by which nitric oxide synthase (NOS) inhibition impacts human sweating is unknow. We tested the hypothesis that the activation of NOS and release on nitric oxide acts to open K+ channels and enhance sweat gland output. Local sweat rate (SR) was measured with a small sweat capsule mounted on the skin while sweating was initiated by intradermal electrical stimulation. Sigmoid shape stimulus-response curves were generated by plotting the area under the SR-time curve versus log10 stimulus frequency and normalized to the peak response during control trials. NOS inhibition alone reduced the peak sweat rate response to 81.5 ± 4.5 % of that seen with lactated Ringers (p = 0.0004). 50 mM TEA alone reduced peak local SR (0.317 ± 0.060 versus 0.511 ± 0.104 mg • min-1 • cm-2 , p = 0.03). Addition of L-NAME following TEA administration produced a further decrease in the peak sweat rate response (p = 0.0145). These data support the hypothesis that sudomotor control of sweat gland activity is locally modulated by a functioning NOS system that appears to be additive and independent to the effect of blockade of K+ channels with TEA.