Roles of eNOS and nNOS in cutaneous vasodilation induced by local warming of the skin and by whole body heat stress in humans

Abstract

We hypothesized that endothelial nitric oxide synthase(eNOS) generation of NO mediates skin vasodilation due to increased local skin temperature(Tloc) and neuronal nitric oxide synthase(nNOS) mediates skin vasodilation due to whole body heat stress(HS). We examined the effects of an eNOS inhibitor, NG‐amino‐L‐arginine(LNAA) and a nNOS inhibitor, N‐omega‐propyl‐L‐arginine(NPLA) on skin blood flow(SkBF) responses to increased Tloc and HS in 2 protocols. In each protocol, 4 microdialysis probes were inserted into skin. SkBF was monitored(LDF). In each protocol, one site was treated with LNAA, another with NPLA, the third with combined LNAA and NPLA(MIX), and the fourth site was untreated. In Protocol 1, LDF/local heating probe holders were used to initially hold Tloc at 34°C and then at 41.5°C. In protocol 2, after a period of normothermia, whole body HS was induced. Results: Protocol‐1: At Tloc=34°C, SkBF did not differ between sites(p>0.05). LNAA and MIX caused similar attenuation of SkBF increases at Tloc=41.5C, but NPLA caused none(p< 0.05 LNAA or MIX vs untreated or NPLA). Protocol‐2: In normothermia, SkBF did not differ between sites(p>0.05). In HS, NPLA and MIX caused similar attenuations of SkBF increases, but LNAA caused none(p< 0.05 NPLA or MIX vs untreated or LNAA). We conclude that eNOS mediates increases in SkBF due to increased Tloc and nNOS mediates increases in SkBF in response to HS.(NIH Grant HL065599)