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

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.

1987 ◽  
Vol 252 (1) ◽  
pp. R181-R187 ◽  
Author(s):  
K. Sato ◽  
F. Sato

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.


1983 ◽  
Vol 245 (2) ◽  
pp. R203-R208 ◽  
Author(s):  
K. Sato ◽  
F. Sato

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.


1979 ◽  
Vol 237 (3) ◽  
pp. C177-C184 ◽  
Author(s):  
K. Sato ◽  
A. Nishiyama ◽  
M. Kobayashi

Contractile properties of an isolated segment of the secretory coil of the monkey palm eccrine sweat gland were studied in vitro with a transducer. Contraction of up to 10 mgf was induced with acetylcholine but not with alpha or beta adrenergic agonists, caffeine, prostaglandin E1, or by a calcium ionophore A23187. Other features included K+ contracture, staircase effect, poor extensibility, length-tension relationship with a peak tensile response at 115--120% of the resting length, and requirement of Ca2+. The function of myoepithelium is unlikely to expulse the preformed sweat because the amount of preformed sweat is small, K+-contracture failed to expulse sweat, and because myoepithelial contraction was not induced by such stimulants of sweat secretion as A23187, phenylephrine, isoproterenol, and prostaglandin E1. The maximal transverse tension of 20 mgf during acetylcholine stimulation under resting tension was calculated to support the luminal hydrostatic pressure of approximately 500 mmHg. Thus the function of the myoepithelium may be to render structural support for the secretory epithelium.


1993 ◽  
Vol 75 (5) ◽  
pp. 2258-2264 ◽  
Author(s):  
K. Sato ◽  
D. E. Timm ◽  
F. Sato ◽  
E. A. Templeton ◽  
D. S. Meletiou ◽  
...  

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.


1994 ◽  
Vol 266 (3) ◽  
pp. R950-R959 ◽  
Author(s):  
K. Sato ◽  
F. Sato

We wished to establish the presence of interleukin-1 (IL-1) in human sweat (5) and clarify its origin and mechanism of secretion. IL-1 alpha concentration ([IL-1 alpha]) in clean sweat from the back increased with the sweat rate, plateauing at the maximal sweat rate ([IL-1 alpha]max). The mean [IL-1 alpha]max was 545 pg/ml (n = 17) for men and 1,324 pg/ml for women in back sweat. The mean [IL-1 alpha]max for axillary sweat in men was 1,568 (n = 6). Palmar sweat was 9.2 ng/ml (n = 5) for IL-1 alpha and 7.9 ng/ml for IL-1 beta. [IL-1 alpha]max decreased to one-third that of the first sweat test, when second sauna sweat tests were conducted after 2 h of continuous sweating on the same day. Western blot analysis of the purified sweat IL-1 alpha fraction revealed bands at 17, 29, and 33 kDa. Immunoreactive IL-1 alpha was localized mainly in the secretory coil lumen, intercellular canaliculi, cytoplasm, mitochondria, and near plasma membranes. Polymerase chain reaction revealed the presence of IL-1 alpha mRNA in the sweat gland and in cultured human eccrine secretory coil cells. Both sweat IL-1 alpha and human recombinant IL-1 alpha at 500 pg/ml strongly stimulated interleukin-6 and interleukin-8 production in cultured fibroblasts. We conclude that the IL-1 alpha-like immunoreactive substance in sweat is IL-1 alpha itself, is derived from the sweat gland, and is biologically active at concentrations normally present in fresh sweat.


2000 ◽  
Vol 48 (3) ◽  
pp. 345-353 ◽  
Author(s):  
Fusako Sato ◽  
Kenzo Sato

Immunoreactive cystic fibrosis transport regulator (CFTR) proteins in human sweat ducts has been documented but CFTR expression in the secretory coil has remained uncertain. Using monoclonal antibodies (MAbs) against epitopes in the R-domain and C-terminus, we observed the following: Formalin fixation masks the CFTR epitopes but the epitopes are exposed by treatment with urea and heat (antigen retrieval). Pen-Fix fixation preserves CFTR epitopes. The secretory coil also expresses CFTR epitopes for the R-domain and C-terminus. An MAb against C-terminus amino acids 1466-1480 coupled to keyhole limpet hemocyanin (MAb WC) stained dark cells predominantly. Staining by MAbs against the C-terminus was completely blocked by a C-terminus peptide. mRNA for CFTR was amplified by RT-PCR in both the duct and the secretory coil. In situ hybridization for CFTR mRNA after 3SR amplification indicates that mRNA is localized in the dark cells and perhaps also in the clear cell cytoplasm near the secretory coil. mRNA is present in both the luminal and basal duct cells. We conclude that CFTR is expressed equally well in both the duct and the secretory coil, suggesting that cAMP-dependent Cl- channels are involved in regulation of sweat secretion and duct absorption.


1990 ◽  
Vol 69 (1) ◽  
pp. 232-236 ◽  
Author(s):  
F. Sato ◽  
M. Owen ◽  
R. Matthes ◽  
K. Sato ◽  
C. V. Gisolfi

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.


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