Endogenous NO decreases cutaneous vasoconstrictor responsiveness during lower‐body negative pressure (LBNP) in the heat stressed individual

Abstract

Previously we reported that, in the heat stressed human, substance(s) presumably released from the cutaneous vasodilator system attenuate the effectiveness of the cutaneous vasoconstrictor system during orthostatic stress. This study tested the hypothesis that endogenous nitric oxide (NO) contributes to the attenuation of the reduction in cutaneous vascular conductance (CVC) during these combined stresses. Two microdialysis probes were placed in dorsal forearm skin of seven healthy volunteers. Skin blood flow was monitored over each microdialysis membrane. CVC was calculated from the ratio of skin blood flow to mean arterial pressure. One membrane was perfused with the NO synthase inhibitor, L-NAME, while the adjacent membrane served as an untreated control site. After internal temperature was elevated ~0.7°C via whole-body heating, 30 mmHg LBNP was applied for 3 min immediately followed by 3 min of 40 mmHg LBNP, or until the onset of presyncopal symptoms. The reduction in CVC during LBNP was significantly greater at the L-NAME treated site relative to the control site (−10.4±7.3 vs. −2.0±7.2%max, P<0.05), despite CVC prior to LBNP being lower at the L-NAME site (48.7±5.2 vs. 58.6±5.9%max, P<0.05). These data suggest that endogenous NO is capable of attenuating the reduction in CVC during an orthostatic challenge of heat stressed humans. Study funded by part by NIH HL61388, HL67422, & HL84072