TEA-sensitive K+ channels and human eccrine sweat gland output

Cholinergic-activated sweating depends on an influx of Ca2+ from extracellular fluid. It is thought that the opening of K+ channels on secretory epithelial cells facilitates Ca2+ entry. We examined the hypothesis that tetraethylammonium (TEA)-sensitive K+ channels participate in sweat production. We used a pre-post experimental design and initiated cholinergic-mediated sweating with intradermal electrical stimulation, monitored local sweat rate (SR) with a small sweat capsule mounted on the skin, and delivered 50 mM TEA via intradermal microdialysis. Local SR was activated by intradermal stimulation frequencies of 0.2–64 Hz, and we generated a sigmoid-shaped stimulus-response curve by plotting the area under the SR-time curve versus log10 stimulus frequency. Peak local SR was reduced from 0.372 ± 0.331 to 0.226 ± 0.190 mg·min−1·cm−2 ( P = 0.0001) during application of 50 mM TEA, whereas the EC50 and Hill slopes were not altered. The global sigmoid-shaped stimulus-response curves for control and 50 mM TEA were significantly different ( P < 0.0001), and the plateau region was significantly reduced ( P = 0.0023) with the TEA treatment. The effect of TEA on peak local SR was similar in male and female subjects. However, we did note a small effect of sex on the shape of the stimulus-response curves during intradermal electrical stimulation. Overall, these data support the hypothesis that cholinergic control of sweat gland activity is modulated by the presence of TEA-sensitive K+ channels in human sweat gland epithelial cells. NEW & NOTEWORTHY The contribution of various potassium channels to the process of cholinergic-mediated human eccrine sweat production is unclear. Using a novel model for cholinergic-mediated sweating in humans, we provide evidence that tetraethylammonium-sensitive K+ channels (KCa1.1 and Kv channels) contribute to eccrine sweat production.

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A model for in vivo analysis of sudomotor sympathetic C-fiber activation and human sweat gland output

Journal of Applied Physiology ◽

10.1152/japplphysiol.01070.2016 ◽

2017 ◽

Vol 123 (2) ◽

pp. 317-325 ◽

Cited By ~ 1

Author(s):

Gary W. Mack

Keyword(s):

Electrical Stimulation ◽

Response Curve ◽

Quantitative Assessment ◽

Sweat Rate ◽

Stimulus Frequency ◽

Time Curve ◽

Stimulus Response ◽

Small Fiber ◽

Local Sweat Rate ◽

C Fiber

Quantitative assessment of small-fiber peripheral neuropathy often involves an evaluation of the interaction between the C-fiber sudomotor nerve and local sweat rate (SR). Typically, some sort of quantitative sudomotor axon reflex test (QSART) is performed to aid in diagnosing small-fiber dysfunction. The currently used QSART demonstrates only moderate test-retest reliability and therefore limits its usefulness in tracking small-fiber dysfunction. A new experimental model to examine small C-fiber function in the skin using intradermal electrical stimulation and simultaneous monitoring of SR is proposed. Using intradermal electrical stimulation (1.5 and 2.5 mA) and varying stimulus frequency from 0.2 to 64 Hz, a quantitative relationship between the area under the SR–time curve and log10 stimulus frequency is modeled using a four-parameter logistic equation, providing the following parameters: baseline, plateau, EC50, and Hill slope. The model has good to excellent repeatability within the same day (ICC = 0.98), on different days at the same skin site (ICC = 0.80), and when comparing two different skin sites (ICC = 0.78) with a small bias estimate and the line of identity always lying within the 95% limits of agreement. Atropine sulfate (0.1 mg/ml) blocked 90 ± 5% of the electrically induced sweating. Overall, the model provides control over sudomotor nerve activity and a quantitative assessment of SR. Finally, the ability to reproduce the quantitative stimulus-response curve on different days allows for a robust assessment of the relationship between the activation of a sympathetic C-fiber and local SR. NEW & NOTEWORTHY A model for quantitative assessment of C-fiber function in human skin using intradermal electrical stimulation and local sweat rate measurements has been developed. This new electrically induced sweating model is nonpainful and allows for a complete stimulus-response curve plotting the area under the local sweat rate-time curve vs. the log10 stimulus frequency. The model has good reproducibility and should provide a means of assessing the progression of small C-fiber peripheral neuropathy in humans.

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Hepatocyte growth factor promoting the proliferation of human eccrine sweat gland epithelial cells is relative to AKT signal channel and β-catenin

Archives of Dermatological Research ◽

10.1007/s00403-011-1167-3 ◽

2011 ◽

Vol 304 (1) ◽

pp. 23-29 ◽

Cited By ~ 5

Author(s):

Xia Lei ◽

Jinjin Wu ◽

Bo Liu ◽

Yuangang Lu

Keyword(s):

Growth Factor ◽

Epithelial Cells ◽

Hepatocyte Growth Factor ◽

Sweat Gland ◽

Eccrine Sweat Gland ◽

Signal Channel ◽

Hepatocyte Growth ◽

Eccrine Sweat

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Effect of physical training on peripheral sweat production

Journal of Applied Physiology ◽

10.1152/jappl.1988.65.2.811 ◽

1988 ◽

Vol 65 (2) ◽

pp. 811-814 ◽

Cited By ~ 84

Author(s):

M. J. Buono ◽

N. T. Sjoholm

Keyword(s):

Physical Training ◽

Sweat Gland ◽

Sweat Rate ◽

Secretory Activity ◽

Sweat Glands ◽

Trained Subjects ◽

Peripheral Mechanism ◽

Sweat Production ◽

Sedentary Women

The purpose of this study was to determine the in vivo secretory activity of sweat glands from sedentary and trained subjects. Peripheral sweat production was determined using pilocarpine iontophoresis in 40 volunteers (10 sedentary men, 10 endurance-trained men, 10 sedentary women, 10 endurance-trained women). Peripheral sweat rate was significantly (P less than 0.05) greater in trained men [6.9 +/- 0.6 (SE) g.m2.min-1] and women (6.1 +/- 0.7) compared with sedentary men (3.1 +/- 0.5) and women (2.5 +/- 0.4). Furthermore, peripheral sweat rate was significantly correlated (r = 0.73) with maximal O2 uptake. The above two findings would suggest that physical training improves the secretory activity of the human sweat gland. Such a result supports previous findings that have suggested that the potentiation in sweating seen after training is achieved via a peripheral mechanism. In addition, several gender-related differences were found in the sudorific response of men and women. Specifically, women have a significantly greater sweat gland density, whereas men have a greater sweat production per gland.

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Electron microscopic finding of eccrine sweat gland epithelial cells in a patient with Krabbe disease

Pediatrics International ◽

10.1111/j.1442-200x.1995.tb03364.x ◽

1995 ◽

Vol 37 (4) ◽

pp. 507-509

Author(s):

ICHIRO OHNO ◽

KAZUKO SHINODA ◽

KEIKO TSUGAWA ◽

NOBORU TAKIZAWA ◽

NOBORU TANIGUCHI ◽

...

Keyword(s):

Epithelial Cells ◽

Sweat Gland ◽

Eccrine Sweat Gland ◽

Krabbe Disease ◽

Electron Microscopic ◽

Microscopic Finding ◽

Electron Microscopic Finding ◽

Eccrine Sweat

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Individual variations in structure and function of human eccrine sweat gland

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1983.245.2.r203 ◽

1983 ◽

Vol 245 (2) ◽

pp. R203-R208 ◽

Cited By ~ 29

Author(s):

K. Sato ◽

F. Sato

Keyword(s):

Sweat Gland ◽

Sweat Rate ◽

Unit Length ◽

Secretory Activity ◽

Eccrine Sweat Gland ◽

Sweat Glands ◽

And Function ◽

Eccrine Sweat

The mechanisms underlying variations in perspiration rate at the glandular level are still poorly understood. Human eccrine sweat glands were dissected from the back of 12 adults, cannulated, and stimulated in vitro with methacholine (Mch). The maximal sweat rate and pKA for Mch determined from the dose-response curve for each individual were compared with the anatomic dimensions of the isolated secretory tubules. There was significant correlation between Mch sensitivity (pKA) and the size of the sweat gland, sweat rate per gland, sweat rate per unit length of the secretory tubule, and sweat rate per unit glandular volume. The sweat glands from individuals judged to be poor sweaters exhibited smaller size, lower secretory activity both in vivo and in vitro, and decreased Mch sensitivity compared with glands from physically fit individuals. We conclude that the increased Mch sensitivity and glandular hypertrophy are the two important features of functionally active sweat glands and infer that these parameters could improve as a result of acclimatization to physical exercise and/or heat.

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Is active sweating during heat acclimation required for improvements in peripheral sweat gland function?

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00253.2009 ◽

2009 ◽

Vol 297 (4) ◽

pp. R1082-R1085 ◽

Cited By ~ 28

Author(s):

Michael J. Buono ◽

Travis R. Numan ◽

Ryan M. Claros ◽

Stephanie K. Brodine ◽

Fred W. Kolkhorst

Keyword(s):

Sweat Gland ◽

Sweat Rate ◽

Heat Acclimation ◽

Whole Body ◽

Moderate Intensity ◽

Sweat Glands ◽

Exercise Heart Rate ◽

Sweat Production ◽

Gland Function ◽

Pilocarpine Iontophoresis

We investigated whether the eccrine sweat glands must actively produce sweat during heat acclimation if they are to adapt and increase their capacity to sweat. Eight volunteers received intradermal injections of BOTOX, to prevent neural stimulation and sweat production of the sweat glands during heat acclimation, and saline injections as a control in the contralateral forearm. Subjects performed 90 min of moderate-intensity exercise in the heat (35°C, 40% relative humidity) on 10 consecutive days. Heat acclimation decreased end-exercise heart rate (156 ± 22 vs. 138 ± 17 beats/min; P = 0.0001) and rectal temperature (38.2 ± 0.3 vs. 37.9 ± 0.3°C; P = 0.0003) and increased whole body sweat rate (0.70 ± 0.29 vs. 1.06 ± 0.50 l/h; P = 0.030). During heat acclimation, there was no measurable sweating in the BOTOX-treated forearm, but the control forearm sweat rate during exercise increased 40% over the 10 days ( P = 0.040). Peripheral sweat gland function was assessed using pilocarpine iontophoresis before and after heat acclimation. Before heat acclimation, the pilocarpine-induced sweat rate of the control and BOTOX-injected forearms did not differ (0.65 ± 0.20 vs. 0.66 ± 0.22 mg·cm−2·min−1). However, following heat acclimation, the pilocarpine-induced sweat rate in the control arm increased 18% to 0.77 ± 0.21 mg·cm−2·min−1 ( P = 0.021) but decreased 52% to 0.32 ± 0.18 mg·cm−2·min−1 ( P < 0.001) in the BOTOX-treated arm. Using complete chemodenervation of the sweat glands, coupled with direct cholinergic stimulation via pilocarpine iontophoresis, we demonstrated that sweat glands must be active during heat acclimation if they are to adapt and increase their capacity to sweat.

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Cysteine proteinase inhibitor in eccrine sweat is derived from sweat gland

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1991.260.2.r314 ◽

1991 ◽

Vol 260 (2) ◽

pp. R314-R320 ◽

Cited By ~ 2

Author(s):

H. Yokozeki ◽

T. Hibino ◽

T. Takemura ◽

K. Sato

Keyword(s):

Liquid Chromatography ◽

Molecular Mass ◽

Sweat Gland ◽

Proteinase Inhibitors ◽

Sweat Rate ◽

Cysteine Proteinase ◽

Sweat Glands ◽

Cysteine Proteinase Inhibitor ◽

Eccrine Sweat

Although cysteine proteinases have been reported to be present in human eccrine sweat, their endogenous inhibitors, cysteine proteinase inhibitors (CPIs), have remained unstudied. We now present evidence that CPIs are indeed a true ingredient of human eccrine sweat. Sweat induced in sauna was collected over a Vaseline barrier placed on the skin to minimize epidermal contamination. The absence of major epidermal contamination of the sweat was further ensured by monitoring an epidermal marker, high-molecular-mass aminopeptidase. Sweat CPI was purified sequentially by chromatography with Sephacryl S-200, carboxymethylated papain-Sepharose, and anion-exchange Mono Q fast-protein liquid chromatography columns. Sweat CPI has a molecular mass of approximately 15 kDa, is stable for temperature (up to 80 degrees C) and pH (from 3 to 10), and inhibits papain, ficin, and sweat cathepsin B- and H-like enzymes. Sweat CPI may be of sweat gland origin because 1) the rate of CPI output in sweat (CPI concentration x sweat rate) is constant over 45 min; 2) antibody against epidermal CPI, which cross-reacts with sweat CPI, localized immunoreactivity in the sweat duct; 3) CPI activity was present in the glandular extracts of control and methacholine-stimulated (for 1 h in vitro) human sweat glands; and 4) the peaks of CPI activity in the glandular extract and sweat CPI were both eluted (by high-pressure liquid chromatography) at around 15 kDa. Sweat CPI may be very similar to epidermal CPI (which belongs to the stefin family of CPIs) because of many shared characteristics. The identity and function of sweat CPI remain to be studied.

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