Generation and transit pathway of H+ is critical for inhibition of palmar sweating by iontophoresis in water

1993 ◽  
Vol 75 (5) ◽  
pp. 2258-2264 ◽  
Author(s):  
K. Sato ◽  
D. E. Timm ◽  
F. Sato ◽  
E. A. Templeton ◽  
D. S. Meletiou ◽  
...  
Keyword(s):  
Sweat Rate ◽  
Tap Water ◽  
Inhibitory Effect ◽  
Sweat Glands ◽  
Galvanic Current ◽  
Silicone Grease ◽  
Secretory Coil ◽  
Cathodal Current ◽  
Palmar Sweating

Passing galvanic current across the skin (known as "tap water iontophoresis" or TWI) inhibits sweating; however, its mechanism of action is unclear. Using improved methods, we confirmed that anodal current has more of an inhibitory effect than cathodal current, water is superior to saline, and the inhibitory effect is a function of the amperage used. To address the importance of current flowing through the pores, a layer of silicone grease was placed on the skin to reduce the shunt pathway across the epidermis. With silicone, total skin conductance decreased 60% without the sweat pores being occluded, swelling of the stratum corneum and collapse of the poral lumen was prevented, and current-induced inhibition of sweating was enhanced, most likely because of an increase in current density in the pores. The pH of anodal water, but not of saline, dropped to 3, whereas that of cathodal water increased to 10 during passage of current through the skin. Acidified anodal water was superior to alkaline water. Sweat glands isolated from TWI-induced anhidrotic palmar skin responded to methacholine in vitro, but the sweat rate and pharmacological sensitivity were slightly lowered. Thus the strong acidity generated by hydrolysis of water in the anodal bath and the further accumulation of H+ in the sweat duct by anodal current may be responsible for TWI-induced inhibition of sweating due to an unknown lesion(s) in the duct or sweat pore. The secretory coil function may also be altered because of exposure to intense acidity during TWI. The importance of H+ movement into the sweat pore for inhibition of sweating could be further exploited to develop new strategies for the control of sweating.

Pharmacologic responsiveness of isolated single eccrine sweat glands

1981 ◽  
Vol 240 (1) ◽  
pp. R44-R51 ◽  
Author(s):  
K. Sato ◽  
F. Sato
Keyword(s):  
Dose Response ◽  
Dissociation Constants ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Adrenergic Agents ◽  
Eccrine Sweat Glands ◽  
Eccrine Sweat

Pharmacologic responsiveness of the eccrine sweat gland has never been studied under well-defined in vitro experimental conditions. Using isolated cannulated single monkey palm eccrine sweat glands, the dose response to both cholinergic and alpha- and beta-adrenergic agents and the effects of various antagonists on agonists were studied. The maximal sweat rate was highest after stimulation with cholinergic agonists, was lower with the beta-adrenergic agonist, and was least with the alpha-adrenergic agonist. Each secretory response was inhibited by its specific antagonist. Attempts to demonstrate the spare receptor, if any, by means of preincubation of the glands with N-(2-chlorethyl)dibenzylamine (Dibenamine) were unsuccessful. From the hyperbolic dose-response curves the values for KA and KB, dissociation constants for agonists and antagonists, respectively, were thus tentatively estimated according to Clark's classical receptor theory. Schild plots for each agonist-antagonist interaction produced straight lines with slopes of near unity, indicating the adequacy of the methodology. It was concluded that the isolated eccrine sweat glands retain their pharmacologic viability in vitro and show responsiveness to cholinergic as well as both alpha- and beta-adrenergic stimulations.

Secretion of Ions and Pharmacological Responsiveness in the Mouse Paw Sweat Gland

1994 ◽  
Vol 86 (2) ◽  
pp. 133-139 ◽  
Author(s):  
K. Sato ◽  
S. Cavallin ◽  
K. T. Sato ◽  
F. Sato
Keyword(s):  
Cyclic Amp ◽  
Sweat Gland ◽  
Sweat Rate ◽  
Eccrine Sweat Gland ◽  
Sweat Secretion ◽  
Cl Channels ◽  
Functional Features ◽  
Secretory Coil ◽  
Rat Paw

1. Some of the basic functional features of the mouse paw eccrine sweat gland were delineated to allow comparison with those of transgenic mice in the future. 2. The mouse sweat secretory coil responds to methacholine, elaborating a K+-rich (> 120 mmol/l), Na+-poor (< 70 mmol/l) primary fluid as does the rat paw sweat gland, as previously reported. The methacholine-induced sweat rate increases with age in parallel with the growth of the sweat gland over the first 6 weeks of life. 3. The sweating response to cyclic AMP-elevating agents, such as isoprenaline or forskolin, is as much as 40% of the methacholine-induced sweat rate at 1 week of age, but falls to 10% by 6 weeks of age despite the fact that the agonist-induced tissue accumulation of cyclic AMP expressed on a per μg of protein basis triples with age over the same period. 4. A marked K+ outflux was also noted in response to methacholine and a small K+ outflux was seen in response to cyclic AMP-elevating agonists in super-fused adult mouse secretory coils in vitro. 5. Since sweat secretion is usually associated with activation of either K+ channels or Cl− channels or both, and since the sweating occurred in response to cyclic AMP-elevating agonists, we speculate that the cyclic AMP-activated Cl− channels (the mouse version of the cystic fibrosis transmembrane conductance regulator) may also occur in the mouse sweat gland, but that the degree of their expression may be influenced by the age of the mice.

Functional and morphological changes in the eccrine sweat gland with heat acclimation

1990 ◽  
Vol 69 (1) ◽  
pp. 232-236 ◽  
Author(s):  
F. Sato ◽  
M. Owen ◽  
R. Matthes ◽  
K. Sato ◽  
C. V. Gisolfi
Keyword(s):  
Relative Humidity ◽  
Heat Tolerance ◽  
Sweat Gland ◽  
Unit Length ◽  
Heat Acclimation ◽  
Tolerance Test ◽  
Sweat Glands ◽  
Before And After ◽  
Secretory Coil

Three adult male patas monkeys (11-15 kg) were heat acclimated by continuous exposure to an ambient temperature of 33 +/- 1 degree C at 13% relative humidity for 9 mo. During the last month, they were also exposed to 45 degrees C at 10% relative humidity for 4 h/day and 5 days/wk. Before and after 3 wk of acclimation, the animals were given a heat-tolerance test in which rectal (Tre) and mean skin (Tsk) temperatures, heart rate, and sweat rate (msw) were monitored during a 90-min exposure to 45 degrees C heat with 24% relative humidity under lenperone (1.0-1.4 mg/kg im) tranquilization. Maximal in vivo msw was also determined in response to subcutaneous injections (1 and 10% solutions) of methacholine (MCh). Before and after 9 wk and 9 mo of acclimation, sweat glands were dissected from biopsy specimens of the lateral calf, cannulated, and stimulated in vitro with MCh. Morphological measurements of isolated tubules were compared with maximal secretory rates produced by MCh stimulation. Three weeks of acclimation 1) reduced Tre and Tsk and increased msw during the heat tolerance test and 2) significantly increased maximal msw in response to MCh stimulation. Acclimation also increased (P less than 0.05) sweat gland size, as measured by tubular length and tubular volume. Maximal in vitro msw produced by MCh stimulation and msw per unit length of secretory coil also increased significantly. We conclude that heat acclimation increases the size of eccrine sweat glands and that these larger glands produce more sweat. They are also more efficient because they produce more sweat per unit length of secretory coil.

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.

Cysteine proteinase inhibitor in eccrine sweat is derived from sweat gland

1991 ◽  
Vol 260 (2) ◽  
pp. R314-R320 ◽  
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.

Role of calcium in cholinergic and adrenergic mechanisms of eccrine sweat secretion

1981 ◽  
Vol 241 (3) ◽  
pp. C113-C120 ◽  
Author(s):  
K. Sato ◽  
F. Sato
Keyword(s):  
Sweat Rate ◽  
Sweat Glands ◽  
Hyperbolic Function ◽  
Ionophore A23187 ◽  
Secretory Rate ◽  
Sweat Secretion ◽  
Eccrine Sweat Glands ◽  
Eccrine Sweat

The role of Ca2+ in eccrine sweat secretion was studied using isolated cannulated monkey palm eccrine sweat glands in vitro. Removal of Ca2+ from the incubation medium promptly abolished sweat secretion induced by methacholine or phenylephrine. In contrast, isoproterenol-induced sweat secretion lasted from 40 to 220 min in a Ca2+-free medium. The methacholine-induced maximal sweat rate was a hyperbolic function of the Ca2+ concentration in the bath and reached a plateau at 1 mM Ca2+. Higher Ca2+ concentrations rather suppressed the secretory rate. The Ca2+ ionophore A23187, but not X537A, at 3 X 10(-6) M induced copious prolonged sweat secretion after a latent period of 10 min. A23187-induced sweat secretion was not inhibited by either atropine or propranolol. D 600 (methoxyverapamil) at 10(-3) M inhibited sweat secretion induced by methacholine or by isoproterenol, although the latter lasted longer than methacholine sweating (20 vs. 5 min) in the presence of D 600. The data support the notion that Ca2+ influx into the cell plays a crucial role in cholinergic and alpha-adrenergic sweating, whereas a partial supply of Ca2+ for isoproterenol-induced sweating is derived from an intracellular store.

Influence of calcium and cyclic nucleotides on beta-adrenergic sweat secretion in equine sweat glands

1984 ◽  
Vol 247 (1) ◽  
pp. C10-C13 ◽  
Author(s):  
J. Bijman ◽  
P. M. Quinton
Keyword(s):  
Cyclic Nucleotides ◽  
Ethylenediaminetetraacetic Acid ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Ionophore A23187 ◽  
Beta Adrenergic ◽  
Cyclic Monophosphate ◽  
Sweat Secretion ◽  
Adrenergic Antagonist

The effects of Ca2+, the cyclic nucleotides adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP), and other parameters of sweat secretion from single equine sweat glands were examined in vitro. Extracellular Ca2+, the Ca2+ ionophore A23187, and the Ca2+ channel antagonist verapamil were all without effect on sweat secretion. Prolonged rinsing of the glands in Ca2+-free Ringer solution with 5 mM ethylenediaminetetraacetic acid decreased the secretion to 30% of the control sweat rate in response to the beta-adrenergic agonist isoproterenol; the sweat response was restored upon adding Ca2+ to the Ringer. cAMP but not cGMP analogues were as effective in stimulating sweat rates as isoproterenol, which elicited maximal secretory rates in vitro. cAMP stimulation was not inhibited by the beta-adrenergic antagonist propranolol. Because the equine sweat gland is predominantly stimulated via the beta-adrenergic receptor, we conclude that cAMP is a principal intracellular messenger in coupling this type of stimulus to the fluid secretion response in this tissue.

In vivo and in vitro characteristics of eccrine sweating in patas and rhesus monkeys

1982 ◽  
Vol 53 (2) ◽  
pp. 425-431 ◽  
Author(s):  
C. V. Gisolfi ◽  
K. Sato ◽  
P. T. Wall ◽  
F. Sato
Keyword(s):  
Rhesus Monkeys ◽  
Sweat Glands ◽  
Sweating Rate ◽  
Eccrine Glands ◽  
Palmar Sweating ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Eccrine Sweat Glands

Biopsy specimens from the chest, palm, back, and lateral calf were obtained from three patas (413;6 kg) and two rhesus monkeys (6 and 8 kg) tranquilized with ketamine hydrochloride (10 mg/kg). The eccrine sweat glands of the specimens were subsequently isolated under a stereomicroscope and prepared for analysis. In both palmar and hairy skin (chest, lateral calf) patas eccrine glands were larger than those isolated from corresponding sites obtained from the rhesus specimens. In vitro stimulation of the patas' glands with methacholine (MCH) chloride produced a dose-dependent increase in sweating rate that was blocked by atropine. Maximal palmar sweating was comparable between the two species of monkey. Mean maximal in vitro sweating rates on the chest and lateral calf of the three patas monkeys were 3.79 and 4.6 nl. gl-1.min-1, respectively. In contrast, the in vitro sweating rate of the rhesus chest glands was negligibly small, i.e., 0.05 nl.gl-1. min-1. Maximal in vivo sweating rates measured by resistance hygrometry during exercise in a hot (40 degrees C) environment were usually synchronous, cyclic, and only slightly below maximal in vitro rates. When the monkey (patas) was already sweating, the onset and cessation of exercise produced an immediate rise and decline in sweating, respectively. At any given rectal or mean skin temperature, sweating was two- to sixfold higher in the patas compared with that of the rhesus monkey. These results indicate that the patas monkey is an excellent model for studying the physiology of sweating in humans.

Differing luminal potential difference of cystic fibrosis and control sweat secretory coils in vitro

1984 ◽  
Vol 247 (4) ◽  
pp. R646-R649 ◽  
Author(s):  
K. Sato
Keyword(s):  
Cystic Fibrosis ◽  
Driving Force ◽  
Potential Difference ◽  
Sweat Glands ◽  
Adrenergic Stimulation ◽  
Human Control ◽  
Secretory Coil ◽  
And Control ◽  
Eccrine Sweat Glands

Transepithelial potential difference (PD) of isolated segments of the secretory coil of both human control and cystic fibrosis (CF) eccrine sweat glands was measured during stimulation with methacholine (MCh) and isoproterenol (ISO) in vitro. Negative luminal PD of about 10 and 16 mV developed across the secretory coil epithelium in control and CF secretory coil, respectively, during maximal MCh stimulation. ISO (10(-5) M) stimulation generated a mean of 1.9-mV negative luminal PD in control glands; however, ISO failed to enhance the luminal PD beyond the resting level of 0.9 mV in the CF secretory coil. The inhibition of ISO-induced (10(-5) M) luminal PD in control secretory coil by propranolol (5 X 10(-5) M) but not by atropine (10(-5) M) indicated its pharmacologic specificity. The possibility is discussed that this lack of electrical driving force during ISO stimulation could be one of the mechanisms for the absence of sweating response to beta-adrenergic stimulation in CF sweat glands reported recently (8). The mechanism for the higher MCh-induced luminal PD in the CF secretory coil remains to be studied.

Sweat secretion by human axillary apoeccrine sweat gland in vitro

1987 ◽  
Vol 252 (1) ◽  
pp. R181-R187 ◽  
Author(s):  
K. Sato ◽  
F. Sato
Keyword(s):  
Sweat Gland ◽  
Sweat Rate ◽  
Fluid Secretion ◽  
Eccrine Sweat Gland ◽  
Sweat Glands ◽  
Clear Fluid ◽  
Apocrine Glands ◽  
Sweat Secretion ◽  
Eccrine Sweat

Functional characteristics of isolated single human axillary apoeccrine sweat glands have been studied using in vitro sweat induction methods. Sustained copious clear fluid secretion was evoked by methacholine (MCh), epinephrine (EP), isoproterenol (ISO), and phenylephrine (PL) in decreasing order in a pharmacologically specific manner. Apoeccrine glands showed a higher cholinergic sensitivity than eccrine sweat glands, as shown by the apparent association constant for MCh of 2.7 X 10(-7) M compared with 2.1 X 10(-6) M for the axillary eccrine sweat gland. The average total sweat rate of the apoeccrine gland for a 30-min period was sevenfold higher than that of the eccrine sweat gland. In contrast, isolated apocrine glands showed intermittent pulsatile turbid sweat secretion in response to MCh or EP. The Na+ and K+ concentration of apoeccrine glands was nearly isotonic, whereas those of apocrine sweat was 120-140 mM for Na+ and 10-20 mM for K+. Apoeccrine ductal Na+ absorption was also observed in the apoeccrine glands and was no more efficient than that of the axillary eccrine sweat gland. Thus apoeccrine sweat glands are functionally and pharmacologically distinct from axillary apocrine glands and significantly contribute to overall axillary sweating in humans.

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