The role of nitric oxide synthase (NOS) inhibition in modulating human thermoregulatory control of sweating and cutaneous dilation was examined in 10 subjects (5 men and 5 women). Three intradermal microdialysis probes were placed in nonglabrous skin of the dorsum of the forearm. The control site was perfused with 0.9% saline, while the two remaining sites were perfused with a nonselective NOS inhibitor: 10 mM N(G)-nitro-L-arginine (L-NAME) or 10 mM N(G)-monomethyl-L-arginine (L-NMMA). Local sweat rate (SR) and skin blood flow (laser-Doppler velocimetry) were monitored directly over the path of the intradermal microdialysis probe while arterial blood pressure was measured in the opposite arm noninvasively. Thermoregulatory responses were induced by cycle ergometer exercise (60% peak oxygen consumption) in a warm environment (30 degrees C). Esophageal temperature increased 1.5 +/- 0.2 degrees C during the 30 min of exercise. The cutaneous dilator response between 5 and 30 min of exercise in the heat was attenuated by both 10 mM L-NAME and 10 mM L-NMMA (P < 0.05). However, 10 mM L-NAME was more effective in blunting the rise in cutaneous vascular conductance during exercise than L-NMMA (P < 0.05). NOS inhibition also reduced the rise in local SR between 10 and 30 min of exercise (P < 0.05). In this case, 10 mM L-NMMA was more effective in limiting the increase in local SR than 10 mM L-NAME (P < 0.05). We conclude that local production of nitric oxide in the skin or around the sweat gland augments local SR and cutaneous dilation during exercise in the heat.

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The role of nitric oxide (NO) in modulating human thermoregulatory sweating was examined in 10 subjects (5 male/5 female). Three intradermal microdialysis probes were placed in the dorsal forearm. The control site was perfused with 0.9% saline while the two remaining sites were perfused with a nitric oxide inhibitor: 10 mM NG‐nitro‐L‐arginine (L‐NAME) or 10 mM NG‐monomethyl‐L‐arginine (L‐NMMA). Local sweat rate (SR) and skin blood flow (SkBF) were monitored directly over the path of the intradermal microdialysis probe while arterial blood pressure was measured in the opposite arm non‐invasively. Thermoregulatory sweating was induced by cycle ergometer exercise (60% VO2max) in a warm environment (30°C). Thermoregulatory control of SR was described by the following four parameters: resting sweat rate (SRREST), the increase in esophageal temperature required to initiate a significant rise in SR (ΔTesTHRESHOLD), the slope of the initial linear rate of rise in SR per unit rise in Tes (SR‐ΔTesSLOPE), and peak SR (SRPEAK). In general, NOS inhibition attenuated thermoregulatory sweating during dynamic exercise in a warm environment as shown in the Table below.L‐NMMA appeared to be more effective, than L‐NAME, in reducing the SR response. We conclude that NO has a subtle but physiologically active role in thermoregulatory control of sweating. (supported by NIH‐RO1‐HL039818)