Does nitric oxide synthase inhibition with L-NMMA reduce cutaneous vasodilation during body heating in humans?
Nitric oxide contributes modestly but inconsistently to cutaneous vasodilation during body heating in humans, indicating it is not the sole factor responsible for dilation.
We sought to examine further the potential role of nitric oxide (NO) in the neurally mediated cutaneous vasodilation in nonacral skin during body heating in humans. Six subjects were heated with a water-perfused suit while cutaneous blood flow was measured by using laser-Doppler flowmeters placed on both forearms. The NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) was given selectively to one forearm via a brachial artery catheter after marked cutaneous vasodilation had been established. During body heating, oral temperature increased by 1.1 +/- 0.1 degreesC while heart rate increased by 30 +/- 6 beats/min. Mean arterial pressure stayed constant at 84 +/- 2 mmHg. In the experimental forearm, cutaneous vascular conductance (CVC; laser-Doppler) decreased to 86 +/- 5% of the peak response to heating (P < 0.05 vs. pre-L-NMMA values) after L-NMMA infusion. In some subjects, L-NMMA caused CVC to fall by approximately 30%; in others, it had little impact on the cutaneous circulation. CVC in the control arm showed a similar increase with heating, then stayed constant while L-NMMA was given to the contralateral side. These results demonstrate that NO contributes modestly, but not consistently, to cutaneous vasodilation during body heating in humans. They also indicate that NO is not the only factor responsible for the dilation.
Shastry et al. (1998) studied this question.