The eNOS antagonist l-NAA attenuated the increase in cutaneous vascular conductance during local skin warming (P<0.05) but not during whole body heat stress (P>0.05).
Does eNOS antagonism with l-NAA attenuate cutaneous vasodilation in response to local heating or whole body heat stress in humans?
eNOS is predominantly responsible for NO generation in human skin during local heating, but not during reflex responses to whole body heat stress.
p-value: p=<0.05
Nitric oxide (NO) participates in locally mediated vasodilation induced by increased local skin temperature (T(loc)) and in sympathetically mediated vasodilation during whole body heat stress. We hypothesized that endothelial NOS (eNOS) participates in the former, but not the latter, response. We tested this hypothesis by examining the effects of the eNOS antagonist N(G)-amino-l-arginine (l-NAA) on skin blood flow (SkBF) responses to increased T(loc) and whole body heat stress. Microdialysis probes were inserted into forearm skin for drug delivery. One microdialysis site was perfused with l-NAA in Ringer solution and a second site with Ringer solution alone. SkBF laser-Doppler flowmetry (LDF) and blood pressure mean arterial pressure (MAP) were monitored, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF / MAP). In protocol 1, T(loc) was controlled with LDF/local heating units. T(loc) initially was held at 34 degrees C and then increased to 41.5 degrees C. In protocol 2, after a normothermic period, whole body heat stress was induced (water-perfused suits). At the end of both protocols, 58 mM sodium nitroprusside was perfused at both microdialysis sites to cause maximal vasodilation for data normalization. In protocol 1, CVC at 34 degrees C T(loc) did not differ between l-NAA-treated and untreated sites (P > 0.05). Local skin warming to 41.5 degrees C T(loc) increased CVC at both sites. This response was attenuated at l-NAA-treated sites (P 0.05). During heat stress, CVC rose to similar levels at l-NAA-treated and untreated sites (P > 0.05). We conclude that eNOS is predominantly responsible for NO generation in skin during responses to increased T(loc), but not during reflex responses to whole body heat stress.
Kellogg et al. (Sat,) conducted a other in Healthy humans. N(G)-amino-l-arginine (l-NAA) vs. Ringer solution alone was evaluated on Cutaneous vascular conductance (CVC) response to increased local skin temperature and whole body heat stress (p=<0.05). The eNOS antagonist l-NAA attenuated the increase in cutaneous vascular conductance during local skin warming (P<0.05) but not during whole body heat stress (P>0.05).