Role of nitric oxide synthase in human sweat gland output.

Abstract

The mechanism by which nitric oxide synthase (NOS) inhibition impacts human sweating is unknown. 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 (LSR) 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 LSR-time curve (LSR AUC) versus log10 stimulus frequency and normalized to the peak AUC response during control trials. NOS inhibition alone reduced the peak sweat rate response to 81.5 ± 4.5% peak LSR AUC of that seen with lactated Ringer's (P = 0.0004). Fifty mM of tetraethylammonium chloride (TEA) alone reduced peak LSR (0.317 ± 0.060 vs. 0.511 ± 0.104 mg·min-1·cm-2, P = 0.03) and the peak LSR AUC response from 0.193 ± 0.170 to 0.158 ± 0.127 mg·cm-2 (P = 0.004). Delivery of a 20 mM nitro-l-arginine methyl ester (l-NAME) following 50 mM TEA produced a further decrease in the peak LSR AUC response to 0.095 ± 0.064 mg·cm-2 (≈20% reduction, 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.NEW & NOTEWORTHY The contribution of nitric oxide synthase (NOS) to the process of cholinergic-mediated human eccrine sweat production is unclear. Using a novel model for cholinergic-mediated sweating in humans, I demonstrate that blocking the NOS system led to a reduction in local sweat rate (LSR). This reduction in LSR was maintained in the presence of K+ channel blockade with tetraethylammonium.