Effect of local acetylcholinesterase inhibition on sweat rate in humans

2001 ◽  
Vol 90 (3) ◽  
pp. 757-762 ◽  
Author(s):  
Manabu Shibasaki ◽  
Craig G. Crandall
Keyword(s):  
Sweat Rate ◽  
Ringer Solution ◽  
Control Site ◽  
Acetylcholinesterase Inhibition ◽  
Whole Body ◽  
Sweat Glands ◽  
Ache Inhibitor ◽  
Temperature Threshold ◽  
Treated Site

ACh is the neurotransmitter responsible for increasing sweat rate (SR) in humans. Because ACh is rapidly hydrolyzed by acetylcholinesterase (AChE), it is possible that AChE contributes to the modulation of SR. Thus the primary purpose of this project was to identify whether AChE around human sweat glands is capable of modulating SR during local application of various concentrations of ACh in vivo, as well as during a heat stress. In seven subjects, two microdialysis probes were placed in the intradermal space of the forearm. One probe was perfused with the AChE inhibitor neostigmine (10 μM); the adjacent membrane was perfused with the vehicle (Ringer solution). SR over both membranes was monitored via capacitance hygrometry during microdialysis administration of various concentrations of ACh (1 × 10−7–2 M) and during whole body heating. SR was significantly greater at the neostigmine-treated site than at the control site during administration of lower concentrations of ACh (1 × 10−7–1 × 10−3 M, P < 0.05), but not during administration of higher concentrations of ACh (1 × 10−2–2 M, P > 0.05). Moreover, the core temperature threshold for the onset of sweating at the neostigmine-treated site was significantly reduced relative to that at the control site. However, no differences in SR were observed between sites after 35 min of whole body heating. These results suggest that AChE is capable of modulating SR when ACh concentrations are low to moderate (i.e., when sudomotor activity is low) but is less effective in governing SR after SR has increased substantially.

scholarly journals Role of Bradykinin Type 2 Receptors in Human Sweat Secretion: Translational Evidence Does Not Support a Functional Relationship

2021 ◽  
Vol 34 (3) ◽  
pp. 162-166
Author(s):  
Thad E. Wilson ◽  
Seetharam Narra ◽  
Kristen Metzler-Wilson ◽  
Artur Schneider ◽  
Kelsey A. Bullens ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Potential Therapeutic Target ◽  
Sweat Secretion ◽  
Hoe 140 ◽  
A Current

Bradykinin increases skin blood flow via a cGMP mechanism but its role in sweating in vivo is unclear. There is a current need to translate cell culture and nonhuman paw pad studies into in vivo human preparations to test for therapeutic viability for disorders affecting sweat glands. Protocol 1: physiological sweating was induced in 10 healthy subjects via perfusing warm (46–48°C) water through a tube-lined suit while bradykinin type 2 receptor (B2R) antagonist (HOE-140; 40 μM) and only the vehicle (lactated Ringer’s) were perfused intradermally via microdialysis. Heat stress increased sweat rate (HOE-140 = +0.79 ± 0.12 and vehicle = +0.64 ± 0.10 mg/cm<sup>2</sup>/min), but no differences were noted with B2R antagonism. Protocol 2: pharmacological sweating was induced in 6 healthy subjects via intradermally perfusing pilocarpine (1.67 mg/mL) followed by the same B2R antagonist approach. Pilocarpine increased sweating (HOE-140 = +0.38 ± 0.16 and vehicle = +0.32 ± 0.12 mg/cm<sup>2</sup>/min); again no differences were observed with B2R antagonism. Last, 5 additional subjects were recruited for various control experiments which identified that a functional dose of HOE-140 was utilized and it was not sudorific during normothermic conditions. These data indicate B2R antagonists do not modulate physiologically or pharmacologically induced eccrine secretion volumes. Thus, B2R agonist/antagonist development as a potential therapeutic target for hypo- and hyperhidrosis appears unwarranted.

Effect of physical training on peripheral sweat production

1988 ◽  
Vol 65 (2) ◽  
pp. 811-814 ◽  
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.

scholarly journals Role of bradykinin type 2 receptors in human sweat secretion: translational evidence does not support a functional relationship

2020 ◽  
Author(s):  
Thad E. Wilson ◽  
Seetharam Narra ◽  
Kristen Metzler-Wilson ◽  
Artur Schneider ◽  
Kelsey A. Bullens ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Potential Therapeutic Target ◽  
Sweat Secretion ◽  
Hoe 140 ◽  
A Current

AbstractBradykinin increases skin blood flow via a cGMP mechanism but its role in sweating in vivo is unclear. There is a current need to translate cell culture and non-human paw pad studies into in vivo human preparations to test for therapeutic viability for disorders affecting sweat glands. Protocol 1: physiological sweating was induced in 10 healthy subjects via perfusing warm (46-48°C) water through a tube-lined suit while bradykinin type 2 receptor (B2R) antagonist (HOE-140; 40 μM) and only the vehicle (lactated Ringer’s) were perfused intradermally via microdialysis. Heat stress increased sweat rate (HOE-140 = +0.79±0.12 and vehicle = +0.64±0.10 mg/cm2/min), but no differences were noted with B2R antagonism. Protocol 2: pharmacological sweating was induced in 6 healthy subjects via intradermally perfusing pilocarpine (1.67 mg/ml) followed by the same B2R antagonist approach. Pilocarpine increased sweating (HOE-140 = +0.38±0.16 and vehicle = +0.32±0.12 mg/cm2/min); again no differences were observed with B2R antagonism. Lastly, 5 additional subjects were recruited for various control experiments which identified that a functional dose of HOE-140 was utilized and it was not sudorific during normothermic conditions. These data indicate B2R antagonists do not modulate physiologically-or pharmacologically-induced eccrine secretion volumes. Thus, B2R agonist/antagonist development as a potential therapeutic target for hypo- and hyperhidrosis appears unwarranted.

scholarly journals Evidence for β-adrenergic modulation of sweating during incremental exercise in habitually trained males

2017 ◽  
Vol 123 (1) ◽  
pp. 182-189 ◽  
Author(s):  
Tatsuro Amano ◽  
Yosuke Shitara ◽  
Naoto Fujii ◽  
Yoshimitsu Inoue ◽  
Narihiko Kondo
Keyword(s):  
Relative Intensity ◽  
Sweat Rate ◽  
Absolute Intensity ◽  
Control Site ◽  
Incremental Exercise ◽  
Saline Control ◽  
Maximum Workload ◽  
Sweat Production ◽  
Adrenergic Mechanism

The aim of the present study was to determine the β-adrenergic contribution to sweating during incremental exercise in habitually trained males. Nine habitually trained and 11 untrained males performed incremental cycling until exhaustion (20 W/min). Bilateral forearm sweat rates (ventilated capsule) were measured at two skin sites that were transdermally administered via iontophoresis with either 1% propranolol (Propranolol, a nonselective β-adrenergic receptor antagonist) or saline (Control). The sweat rate was evaluated as a function of both relative (percentage of maximum workload) and absolute exercise intensities. The sweat rate at the Propranolol site was lower than the control during exercise at 80 (0.57 ± 0.21 and 0.45 ± 0.19 mg·cm−2·min−1 for Control and Propranolol, respectively) and 90% (0.74 ± 0.22 and 0.65 ± 0.17 mg·cm−2·min−1, respectively) of maximum workload in trained males (all P < 0.05). By contrast, no between-site differences in sweat rates were observed in untrained counterparts (all P > 0.05). At the same absolute intensity, higher sweat rates on the control site were observed in trained males relative to the untrained during exercise at 160 (0.23 ± 0.20 and 0.04 ± 0.05 mg·cm−2·min−1 for trained and untrained, respectively) and 180 W (0.40 ± 0.20 and 0.13 ± 0.13 mg·cm−2·min−1, respectively) (all P < 0.05), whereas this between-group difference was not observed at the Propranolol site (all P > 0.05). We show that the β-adrenergic mechanism does modulate sweating during exercise at a submaximal high relative intensity in habitually trained males. The β-adrenergic mechanism may in part contribute to the greater sweat production in habitually trained males than in untrained counterparts during exercise. NEW & NOTEWORTHY We demonstrated for the first time that the β-adrenergic mechanism does modulate sweating (i.e., β-adrenergic sweating) during exercise using a localized β-adrenoceptor blockade in humans in vivo. β-Adrenergic sweating was evident in habitually trained individuals during exercise at a submaximal high relative intensity (80–90% maximal work). This observation advances our understanding of human thermoregulation during exercise and of the mechanism that underlies sweat gland adaptation to habitual exercise training.

Individual variations in structure and function of human eccrine sweat gland

1983 ◽  
Vol 245 (2) ◽  
pp. R203-R208 ◽  
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.

Skin tattooing impairs sweating during passive whole body heating

2020 ◽  
Vol 129 (5) ◽  
pp. 1033-1038
Author(s):  
Maurie J. Luetkemeier ◽  
Dustin R. Allen ◽  
Mu Huang ◽  
Faith K. Pizzey ◽  
Iqra M. Parupia ◽  
...  
Keyword(s):  
Sweat Rate ◽  
Whole Body ◽  
Sweat Glands ◽  
Moderate Increase ◽  
The Novel ◽  
Cholinergic Stimulation ◽  
Whole Body Heat Stress ◽  
Reflex Control ◽  
Body Heat ◽  
Eccrine Sweat Glands

This study is the first to assess the reflex control of sweating in tattooed skin. The novel findings are twofold. First, attenuated increases in sweat rate were observed in tattooed skin compared with adjacent healthy non-tattooed skin in response to a moderate increase (1.0°C) in internal temperature during a passive whole body heat stress. Second, reduced sweating in tattooed skin is likely related to functional damage to the secretory mechanisms of eccrine sweat glands, rendering it less responsive to cholinergic stimulation.

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

2009 ◽  
Vol 297 (4) ◽  
pp. R1082-R1085 ◽  
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.

Control of internal temperature threshold for active cutaneous vasodilation by dynamic exercise

1991 ◽  
Vol 71 (6) ◽  
pp. 2476-2482 ◽  
Author(s):  
D. L. Kellogg ◽  
J. M. Johnson ◽  
W. A. Kosiba
Keyword(s):  
Sweat Rate ◽  
Bicycle Ergometer ◽  
Dew Point ◽  
Whole Body ◽  
Temperature Threshold ◽  
Internal Temperature ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Temperature Thresholds ◽  
Ergometer Exercise

Exercise induces shifts in the internal temperature threshold at which cutaneous vasodilation begins. To find whether this shift is accomplished through the vasoconstrictor system or the cutaneous active vasodilator system, two forearm sites (0.64 cm2) in each of 11 subjects were iontophoretically treated with bretylium tosylate to locally block adrenergic vasoconstrictor control. Skin blood flow was monitored by laser-Doppler flowmetry (LDF) at those sites and at two adjacent untreated sites. Mean arterial pressure (MAP) was measured noninvasively. Cutaneous vascular conductance was calculated as LDF/MAP. Forearm sweat rate was also measured in seven of the subjects by dew point hygrometry. Whole body skin temperature was raised to 38 degrees C, and supine bicycle ergometer exercise was then performed for 7–10 min. The internal temperature at which cutaneous vasodilation began was recorded for all sites, as was the temperature at which sweating began. The same subjects also participated in studies of heat stress without exercise to obtain vasodilator and sudomotor thresholds from rest. The internal temperature thresholds for cutaneous vasodilation were higher during exercise at both bretylium-treated (36.95 +/- 0.07 degrees C rest, 37.20 +/- 0.04 degrees C exercise, P less than 0.05) and untreated sites (36.95 +/- 0.06 degrees C rest, 37.23 +/- 0.05 degrees C exercise, P less than 0.05). The thresholds for cutaneous vasodilation during rest or during exercise were not statistically different between untreated and bretylium-treated sites (P greater than 0.05). The threshold for the onset of sweating was not affected by exercise (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence of functional beta-adrenoceptors in the cutaneous vasculature

1997 ◽  
Vol 273 (2) ◽  
pp. H1038-H1043 ◽  
Author(s):  
C. G. Crandall ◽  
R. A. Etzel ◽  
J. M. Johnson
Keyword(s):  
Blood Flow ◽  
Ringer Solution ◽  
The Other ◽  
Whole Body ◽  
Beta Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Cutaneous Vasodilation ◽  
Adrenoceptor Agonist ◽  
Treated Site

During a hyperthermic challenge, skin blood flow (SkBF) increases primarily through activation of the cutaneous active vasodilator system. However, mechanisms through which activation of this system elevates SkBF remain unknown. In this project, we sought to identify whether functional beta-adrenoceptors exist on cutaneous vessels and, if present, whether these receptors play an important role in elevating SkBF during a hyperthermic challenge. In protocol 1, SkBF was assessed over two intradermal microdialysis probes. Initially, both probes were perfused with lactated Ringer solution. Probe A was then perfused with a 200 microM solution of the beta-adrenoceptor agonist isoproterenol while probe B was perfused with a 1.7 mM solution of the beta-adrenoceptor antagonist propranolol. Isoproterenol perfusion significantly increased SkBF from 17.7 +/- 2.4 to 70.8 +/- 13.2 perfusion units (PU; P < 0.05), whereas propranolol perfusion did not significantly affect SkBF (23.4 +/- 6.5 to 27.0 +/- 6.8 PU; P > 0.05). After this period, the solutions perfusing the probes were switched. Isoproterenol did not significantly change SkBF at the propranolol-treated site (27.0 +/- 6.8 to 26.4 +/- 7.5 PU; P < 0.05). In protocol 2, SkBF was assessed over two microdialysis probes during indirect whole body heating. One probe was perfused with Ringer solution while the other probe was perfused with 1.7 mM propranolol. The degree of elevation in SkBF during heat stress at the propranolol-treated site (10.4 +/- 1.5 to 35.8 +/- 3.1 PU) was similar to the elevation in SkBF at the Ringer solution site (11.6 +/- 1.0 to 35.0 +/- 1.2 PU). These data demonstrate the presence of functional beta-adrenoceptors in the skin; however, these receptors play no significant role in mediating cutaneous vasodilation during indirect whole body heating.

Mean body temperature does not modulate eccrine sweat rate during upright tilt

2005 ◽  
Vol 98 (4) ◽  
pp. 1207-1212 ◽  
Author(s):  
Thad E. Wilson ◽  
Jian Cui ◽  
Craig G. Crandall
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
Peroneal Nerve ◽  
Sweat Rate ◽  
Control Site ◽  
Body Temperatures ◽  
Mean Body Temperature ◽  
Head Up Tilt ◽  
Treated Site ◽  
Eccrine Sweat

Conflicting reports exist about the role of baroreflexes in efferent control of eccrine sweat rate. These conflicting reports may be due to differing mean body temperatures between studies. The purpose of this project was to test the hypothesis that mean body temperature modulates the effect of head-up tilt on sweat rate and skin sympathetic nerve activity (SSNA). To address this question, mean body temperature (0.9·internal temperature + 0.1·mean skin temperature), SSNA (microneurography of peroneal nerve, n = 8), and sweat rate (from an area innervated by the peroneal nerve and from two forearm sites, one perfused with neostigmine to augment sweating at lower mean body temperatures and the second with the vehicle, n = 12) were measured in 13 subjects during multiple 30° head-up tilts during whole body heating. At the end of the heat stress, mean body temperature (36.8 ± 0.1 to 38.0 ± 0.1°C) and sweat rate at all sites were significantly elevated. No significant correlations were observed between mean body temperature and the change in SSNA during head-up tilt ( r = 0.07; P = 0.62), sweating within the innervated area ( r = 0.06; P = 0.56), sweating at the neostigmine treated site ( r = 0.04; P = 0.69), or sweating at the control site ( r = 0.01; P = 0.94). Also, for each tilt throughout the heat stress, there were no significant differences in sweat rate (final tilt sweat rates were 0.69 ± 0.11 and 0.68 ± 0.11 mg·cm−2·min−1 within the innervated area; 1.04 ± 0.16 and 1.06 ± 0.16 mg·cm−2·min−1 at the neostigmine-treated site; and 0.85 ± 0.15 and 0.85 ± 0.15 mg·cm−2·min−1 at the control site, for supine and tilt, respectively). Hence, these data indicate that mean body temperature does not modulate eccrine sweat rate during baroreceptor unloading induced via 30° head-up tilt.

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