Plasma hyperosmolality attenuates skin sympathetic nerve activity during passive heat stress in humans

摘要: Key points Plasma hyperosmolality delays the onset for sweat production and cutaneous vasodilatation during heat stress in humans; however, mechanism by which exerts this effect remains unknown. This study examined if plasma a central and/or peripheral modulation of thermoregulatory function humans. The main findings are that increase skin sympathetic nerve activity whole-body passive humans. In contrast, local intradermal infusion hyperosmotic saline did not affect sweating or vasodilatation. These results suggest threshold inhibiting efferent humans. Abstract In humans, stress. However, it unknown through (i.e. CNS) effector organ) activity. We intravenous affects (SSNA) heating healthy Furthermore, we heating. Following either 0.9% (ISO) 3.0% (HYPER) NaCl saline, 12 subjects were passively heated until core temperature increased ∼0.6°C. During each condition, vascular conductance measured over two microdialysis probes, one perfused with ISO other HYPER saline. Intravenous osmolality (294 ± 3 to 316 ± 5 mOsm kg–1 H2O, P ≤ 0.01), remained greater than throughout Plasma delayed mean body (+1.24 ± 0.18 vs. +1.60 ± 0.18°C, P ≤ 0.01) (+1.15 ± 0.18 vs. +1.53 ± 0.22°C, attenuated SSNA (+147 ± 178 vs. +427 ± 281%, P ≤ 0.01). Intradermal baseline (P ≤ 0.01), further subsequent period (P = 0.11). (P = 0.99). These provide direct evidence modulatory governing