Nitric oxide mediates increases in skin blood flow during local warming in humans

Local warming of skin induces vasodilation by unknown mechanisms. To test whether nitric oxide(NO) is required for such increases in skin blood flow(SkBF), we examined effects of NO-synthase(NOS) inhibition with L-nitro-arginine methylester (L-NAME) on vasodilation induced by local warming of skin in 5 subjects. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of L-NAME or Nitroprusside. SkBF was monitored by laser-Doppler flowmetry(LDF) at microdialysis sites. Local temperature(Tloc) at both sites was controlled with special LDF probe holders. Mean arterial pressure(MAP, Finapres) was measured and cutaneous vascular conductance calculated(CVC=LDF/MAP). Data collection began with a 10 minute control periodá(Tloc at both sites=34°C). One site was then warmed to 41°C while the second was maintained at 34°C throughout the study. Local warming of the skin increased CVC by 377±136%(p<0.01). L-NAME administration reduced CVC to 217±62% of control(p>0.05 vs control, p<0.05 vs heating), despite the elevation of Tloc. Subsequent administration of Nitroprusside increased CVC to levels no different than those induced by local warming alone. At a Tloc of 34°, L-NAME had no significant effect on CVC; however, Nitroprusside administration increased CVC by 443±57%(p<0.01). Thus, NOS inhibition reduced, and Nitroprusside restored, the cutaneous vasodilation induced by elevation of Tloc. We conclude that the mechanism of vasodilation by local warming of the skin requires NO generation by NOS.