Evidence Against nNOS Participation in Vasodilation Induced by Local Warming of the Skin in Humans

Nitric oxide (NO) participates in the vasodilation induced by increased local skin temperature (Tloc). We hypothesized neuronal nitric oxide synthase (nNOS) is a source of NO during local skin warming. We examined the effects of a specific nNOS inhibitor, 7‐nitro‐indazole (7NI) on increases in skin blood flow (SkBF) caused by increased Tloc. Three microdialysis probes (MD) were inserted into forearm skin. Skin blood flow (SkBF) was monitored by Laser‐Doppler Flowmetry (LDF) at MD sites. Local temperatures at the MD sites were controlled by specialized LDF probe‐holder/local‐heater units. The study began with perfusion Ringer’s at one MD site, 5% DMSO/Ringers at a 2 nd site, and 2mM 7NI in 5% DMSO/Ringers at the 3 rd site. (2mM 7NI was previously shown to attenuate SkBF increases during whole body heat stress.) In the protocol, Tloc was initially held at 34°C and then was raised to 41.5°C to cause local vasodilation. Finally, 58mM nitroprusside was perfused at all MD sites to cause maximal vasodilation for data normalization. No SkBF differences were found between sites with Tloc=34°C (p>0.05 between sites). SkBF dilated at all sites as Tloc was increased (p<0.05 vs Tloc=34C)). No SkBF differences were found between sites with Tloc=41.5°C (p>0.05 between sites). We conclude that the nNOS isoform does not participate in the vasodilation induced by local warming of the skin. (supported by NIH Grant HL065599)