Sweat, the driving force behind normal skin: An emerging perspective on functional biology and regulatory mechanisms

Murota, Hiroyuki; Matsui, Saki; Ono, Emi; Kijima, Akiko; Kikuta, Junichi; Ishii, Masaru; Katayama, Ichiro

doi:10.1016/j.jdermsci.2014.08.011

Cited by 69 publications

(63 citation statements)

References 44 publications

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“…Such changes in osmolality could affect ion flux at the level of the secretory coil and ion re‐absorption at the level of the duct, which are critical for normal sweat production (Murota et al . ). We therefore hypothesized that intradermal infusion of hyperosmotic saline would attenuate sweat production during passive heating.…”

Section: Discussionmentioning

confidence: 97%

“…As sweat production is governed by ion flux at the level of the secretory coil and ion re‐absorption at the level of the duct (Murota et al . ), greater osmolality of the fluid surrounding the sweat gland may affect ion flux and/or re‐absorption and therefore sweat production independent of any potential central influence. Furthermore, intradermal infusion of hyperosmotic saline attenuates cutaneous vasodilatation during local heating (DuPont et al .…”

Section: Introductionmentioning

confidence: 99%

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

Gagnon

Romero

Ngo

et al. 2015

The Journal of Physiology

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Key pointsr Plasma hyperosmolality delays the onset for sweat production and cutaneous vasodilatation during heat stress in humans; however, the mechanism by which hyperosmolality exerts this effect remains unknown.r This study examined if plasma hyperosmolality exerts a central and/or peripheral modulation of thermoregulatory function in humans.r The main findings are that plasma hyperosmolality delays the increase in skin sympathetic nerve activity during whole-body passive heat stress in humans. In contrast, local intradermal infusion of hyperosmotic saline did not affect sweating or cutaneous vasodilatation.r These results suggest that plasma hyperosmolality delays the onset threshold for sweating and cutaneous vasodilatation by inhibiting efferent thermoregulatory activity in humans.Abstract In humans, plasma hyperosmolality delays the onset of sweating and cutaneous vasodilatation during heat stress. However, it remains unknown if hyperosmolality exerts this effect through a central (i.e. CNS) and/or peripheral (i.e. effector organ) modulation of thermoregulatory activity. We examined if intravenous infusion of hyperosmotic saline affects skin sympathetic nerve activity (SSNA) during whole-body passive heating in healthy humans. Furthermore, we examined if local intradermal infusion of hyperosmotic saline affects sweating and cutaneous vasodilatation during passive heating. Following intravenous infusion of either 0.9% (ISO) or 3.0% (HYPER) NaCl saline, 12 subjects were passively heated until core temperature increased by ß0.6°C. During each condition, sweating and cutaneous vascular conductance were measured over two intradermal microdialysis probes, one perfused with ISO saline and the other with HYPER saline. Intravenous infusion of HYPER saline increased plasma osmolality (294 ± 3 to 316 ± 5 mOsm kg -1 H 2 O, P ࣘ 0.01), which remained greater than ISO throughout heating. Plasma hyperosmolality delayed the mean body temperature onset of sweating (+1.24 ± 0.18 vs. +1.60 ± 0.18°C, P ࣘ 0.01) and cutaneous vasodilatation (+1.15 ± 0.18 vs. +1.53 ± 0.22°C, P ࣘ 0.01), and attenuated the increase in SSNA during heating (+147 ± 178 vs. +427 ± 281%, P ࣘ 0.01). Intradermal infusion of HYPER saline increased baseline cutaneous vascular conductance (P ࣘ 0.01), which did not increase further during the subsequent heating period (P = 0.11). In contrast, intradermal infusion of HYPER saline did not affect sweating (P = 0.99). These results provide direct evidence that plasma hyperosmolality exerts a central modulatory effect governing efferent thermoregulatory activity in humans. Abbreviations HYPER, hyperosmotic; ISO, iso-osmotic; SSNA, skin sympathetic nerve activity.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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

Gagnon

Romero

Ngo

et al. 2015

The Journal of Physiology

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“…For example, PAR‐2 is also expressed in NCL‐SG3 cells, and activation of PAR‐2 by trypsin‐like serine proteases increased Ca 2+ concentrations in cytosol and enhanced chloride secretion . In addition, histamine was recently shown to inhibit sweat secretion by suppressing phosphorylation of GSK3 β , which is a target for phosphorylation by acetylcholine . This may hint at an uncharacterized mechanism involving glycogen levels in sweat secretion.…”

Section: Mechanism Of Sweat Secretionmentioning

confidence: 99%

Eccrine sweat gland development and sweat secretion

Cui

Schlessinger

2015

Experimental Dermatology

154

173

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Eccrine sweat glands help to maintain homoeostasis, primarily by stabilizing body temperature. Derived from embryonic ectoderm, millions of eccrine glands are distributed across human skin and secrete litres of sweat per day. Their easy accessibility has facilitated the start of analyses of their development and function. Mouse genetic models find sweat gland development regulated sequentially by Wnt, Eda and Shh pathways, although precise subpathways and additional regulators require further elucidation. Mature glands have two secretory cell types, clear and dark cells, whose comparative development and functional interactions remain largely unknown. Clear cells have long been known as the major secretory cells, but recent studies suggest that dark cells are also indispensable for sweat secretion. Dark cell-specific Foxa1 expression was shown to regulate a Ca2+-dependent Best2 anion channel that is the candidate driver for the required ion currents. Overall, it was shown that cholinergic impulses trigger sweat secretion in mature glands through second messengers – for example InsP3 and Ca2+ – and downstream ion channels/transporters in the framework of a Na+-K+-Cl− cotransporter model. Notably, the microenvironment surrounding secretory cells, including acid–base balance, was implicated to be important for proper sweat secretion, which requires further clarification. Furthermore, multiple ion channels have been shown to be expressed in clear and dark cells, but the degree to which various ion channels function redundantly or indispensably also remains to be determined.

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“…Beyond unambiguously showing aggravation of histamine-induced neurogenic flare starting at 2 min post-histamine pricks and lasting throughout the assessment period, this study also showed a significantly increased sudomotor activity on the fingertips during the conditioning pain stimulation indicative of increased sympathetic efferent fiber activity. The decrease in skin conductance within the prick area suggests a local histamine-induced desiccation of the skin immediately around the prick site (which was offset by a slight increase evoked by pressure conditioning stimulation), in line with the known hypohydrotic effect of histamine (Matsui et al 2014a(Matsui et al , 2014bMurota et al 2015).…”

Section: The Neurogenic Inflammatory Response Is Increased By Heterotmentioning

confidence: 58%

Conditioning pain stimulation does not affect itch induced by intra-epidermal histamine pricks but aggravates neurogenic inflammation in healthy volunteers

Andersen

Imai

Petersen

et al. 2016

Somatosensory & Motor Research

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This study investigated whether itch induced by intra-epidermal histamine is subjected to modulation by a standardized conditioned pain modulation (CPM) paradigm in 24 healthy volunteers. CPM was induced by computer-controlled cuff pressure algometry and histamine was introduced to the volar forearm by skin prick test punctures. Moreover, neurogenic inflammation and wheal reactions induced by histamine and autonomic nervous system responses (heart rate variability and skin conductance) were monitored. CPM did not modulate the intensity of histamine-induced itch suggesting that pruriceptive signaling is not inhibited by pain-recruited endogenous modulation, however, CPM was found to aggravate histamine-induced neurogenic inflammation, likely facilitated by efferent sympathetic fibers.

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Sweat, the driving force behind normal skin: An emerging perspective on functional biology and regulatory mechanisms

Cited by 69 publications

References 44 publications

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

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

Eccrine sweat gland development and sweat secretion

Conditioning pain stimulation does not affect itch induced by intra-epidermal histamine pricks but aggravates neurogenic inflammation in healthy volunteers

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