We tested the hypothesis that local heating induced nitric oxide (NO) production attenuates cutaneous vasoconstrictor responsiveness. Eleven subjects had 4 microdialysis membranes placed in forearm skin. Two membranes were perfused with 10 mM of NG-nitro-L-arginine (L-NAME) and two with Ringers solution (Control) and all sites were locally heated to 34 °C. Subjects then underwent 5 min of 60 mmHg lower-body negative pressure (LBNP). Two sites (a Control and an L-NAME site) were then heated to 39 °C, while the other two sites were heated to 42 °C. At the L-NAME sites, skin blood flow was elevated using 0.75-2 mg.ml^-1 of adenosine in the perfusate solution (ADN+L-NAME) similar to Control sites. Subjects then underwent another 5 min of 60 mmHg LBNP. At 34 °C, cutaneous vascular conductance (CVC) decreased similarly at both control and L-NAME sites during LBNP ( 7.9±3.0 and 3.4±0.8 %max, respectively, P > 0.05). The reduction in CVC to LNBP was also similar between Control and ADN + L-NAME sites at 39 °C (Control 11.4±2.5 % vs AND+L-NAME 7.9±2.0 %max, P > 0.05) and 42 °C (Control 1.9±2.7 vs ADN+L-NAME 4.2±2.7 %max, P > 0.05). However, the decrease in CVC at 42 °C, regardless of site, was smaller than at 39 °C (P < 0.05). These results do not support the hypothesis that local heating induced NO production attenuates cutaneous vasoconstrictor responsiveness during high levels of LBNP. However, elevated local temperature, per se, attenuates cutaneous vasoconstrictor responsiveness to LBNP, presumably through non-NO mechanisms.