Effect of VIP on sweat secretion and cAMP accumulation in isolated simian eccrine glands

1987 ◽  
Vol 253 (6) ◽  
pp. R935-R941 ◽  
Author(s):  
K. Sato ◽  
F. Sato
Keyword(s):  
Functional Significance ◽  
Time Course ◽  
Sweat Rate ◽  
Camp Level ◽  
Sweat Glands ◽  
Camp Accumulation ◽  
Eccrine Glands ◽  
Sweat Secretion ◽  
Eccrine Sweat Glands ◽  
Eccrine Sweat

Although vasoactive intestinal peptide (VIP)-immunoreactive nerves have been identified around the eccrine sweat glands, their functional significance is unknown. We found that VIP evokes eccrine sweat secretion in isolated monkey palm eccrine sweat glands in vitro as profusely as does isoproterenol (Iso), however, at concentrations two orders of magnitude lower than that of Iso. Like Iso sweating, the VIP sweating was relatively insensitive to removal of Ca2+ from the medium. The time course of adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in the secretory coil paralleled that of sweat secretion. However, unlike Iso stimulations, both VIP-induced cAMP level and VIP sweat rate markedly declined with time. The attenuation of VIP sweat rate was reversed by forskolin and by theophylline, suggesting that the attenuation is caused partially by desensitization of the receptor-cyclase complex and/or by cAMP breakdown by phosphodiesterase. Forskolin stimulated the VIP-induced cAMP level more than can be expected from a simple additive effect. The sudorific effects of a submaximal concentration of VIP (6 X 10(-9) M) and that of methacholine (MCh) (10(-8) M) were only additive. The VIP-induced cAMP level was markedly augmented by MCh and further enhanced by Iso with or without theophylline. Thus the most salient biochemical consequence of the VIP-ergic component of sweat gland innervation is to induce synergistic amplification of tissue cAMP accumulation. The functional significance of synergistically accumulated cAMP in physiological eccrine sweating remains to be studied.

Cyclic GMP accumulation during cholinergic stimulation of eccrine sweat glands

1984 ◽  
Vol 247 (3) ◽  
pp. C234-C239 ◽  
Author(s):  
K. Sato ◽  
F. Sato
Keyword(s):  
Time Course ◽  
Sweat Glands ◽  
Cgmp Level ◽  
Ionophore A23187 ◽  
Cholinergic Stimulation ◽  
Sweat Secretion ◽  
Transient Elevation ◽  
Eccrine Sweat Glands ◽  
Eccrine Sweat

The possibility that guanosine 3'5'-cyclic monophosphate (cGMP) may be an intracellular mediator of cholinergic stimulation [methacholine chloride (MCh)] was explored by comparing the relationship between the time course of cGMP accumulation and sweat secretion by use of isolated monkey palm eccrine sweat glands. Isolated sweat glands were incubated with MCh or other agents, and tissue levels of cGMP were determined by radioimmunoassay. In parallel experiments, sweat secretion was induced from cannulated single sweat glands in vitro. Stimulation with MCh produced a Ca-dependent transient elevation of cGMP level from 10 to 80 fmol/gland, peaking at 1-2 min but returning to the basal level by 5 min. The MCh-induced cGMP level was dose dependent and was inhibited by atropine. Ionophore A23187 (2 X 10(-4) M), however, caused persistent elevation of cGMP level for at least 20 min. Neither 10(-4) M MNNG, which elevated the cGMP level comparably with MCh stimulation, nor 8-bromo-cGMP (2 mM) induced sweat secretion. Thus although a parallelism between the cGMP level and sweating rate appears to hold for the initial stage of MCh-induced sweating, it does not hold for the steady state of sweat secretion. Data could not be interpreted to favor the notion that cGMP may be the intracellular mediator of cholinergic sweat secretion.

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.

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.

Cholinergic potentiation of isoproterenol-induced cAMP level in sweat gland

1983 ◽  
Vol 245 (3) ◽  
pp. C189-C195 ◽  
Author(s):  
K. Sato ◽  
F. Sato
Keyword(s):  
Camp Level ◽  
Sweat Glands ◽  
Maximal Response ◽  
Ionophore A23187 ◽  
Dependent Manner ◽  
Camp Accumulation ◽  
Major Mechanism ◽  
Agonist Concentration ◽  
Dose Dependent ◽  
Eccrine Sweat Glands

Although methacholine (MCh) and a Ca2+ ionophore A23187 do not enhance the tissue adenosine 3',5'-cyclic monophosphate (cAMP) level by themselves, they markedly potentiate isoproterenol (ISO)-induced tissue cAMP accumulation in isolated simian eccrine sweat glands in a dose-dependent manner. The agonist concentration producing 50% of the maximal response of such a potentiated cAMP accumulation was 2.1 X 10(-7) M for MCh, 2.5 X 10(-7) M for ISO, and 2.9 X 10(-6) M for A23187. Unlike cAMP accumulation induced by ISO alone, MCh-stimulated ISO-induced cAMP accumulation is dependent on extracellular Ca2+. MCh- plus ISO-induced cAMP level is tripled by 10(-2) M theophylline (TH), and while the ISO-induced cAMP level was also elevated by TH, it was not enhanced to the level of ISO-plus MCh-induced cAMP accumulation, indicating that phosphodiesterase inhibition is not the major mechanism for the augmentative effect of MCh. The augmentative effect of MCh was seen only in the secretory portion, whereas that of A23187 was seen in both the secretory portion and the duct. The data suggest that MCh-induced augmentation of ISO-stimulated cAMP accumulation is due to increased cAMP formation, not decreased cAMP degradation, and that it may be mediated by an elevated intracellular Ca2+.

Neural control and mechanisms of eccrine sweating during heat stress and exercise

2006 ◽  
Vol 100 (5) ◽  
pp. 1692-1701 ◽  
Author(s):  
Manabu Shibasaki ◽  
Thad E. Wilson ◽  
Craig G. Crandall
Keyword(s):  
Heat Stress ◽  
Neural Control ◽  
Sweat Glands ◽  
Past Century ◽  
Evaporative Heat Loss ◽  
Sweat Secretion ◽  
Prolonged Heat ◽  
Skin Temperatures ◽  
Eccrine Sweat Glands ◽  
Eccrine Sweat

In humans, evaporative heat loss from eccrine sweat glands is critical for thermoregulation during exercise and/or exposure to hot environmental conditions, particularly when environmental temperature is greater than skin temperature. Since the time of the ancient Greeks, the significance of sweating has been recognized, whereas our understanding of the mechanisms and controllers of sweating has largely developed during the past century. This review initially focuses on the basic mechanisms of eccrine sweat secretion during heat stress and/or exercise along with a review of the primary controllers of thermoregulatory sweating (i.e., internal and skin temperatures). This is followed by a review of key nonthermal factors associated with prolonged heat stress and exercise that have been proposed to modulate the sweating response. Finally, mechanisms pertaining to the effects of heat acclimation and microgravity exposure are presented.

scholarly journals Determination of the maximum rate of eccrine sweat glands’ ion reabsorption using the galvanic skin conductance to local sweat rate relationship

2015 ◽  
Vol 116 (2) ◽  
pp. 281-290 ◽  
Author(s):  
Tatsuro Amano ◽  
Nicola Gerrett ◽  
Yoshimitsu Inoue ◽  
Takeshi Nishiyasu ◽  
George Havenith ◽  
...  
Keyword(s):  
Skin Conductance ◽  
Maximum Rate ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Local Sweat Rate ◽  
Rate Relationship ◽  
Eccrine Sweat Glands ◽  
Eccrine Sweat

Spontaneous sweat secretion in calcium-free strontium medium

1982 ◽  
Vol 242 (5) ◽  
pp. C353-C359 ◽  
Author(s):  
K. Sato ◽  
F. Sato
Keyword(s):  
Bath Temperature ◽  
Anticholinergic Effect ◽  
Sweat Glands ◽  
Membrane Channels ◽  
Saturation Function ◽  
Sweat Secretion ◽  
Eccrine Sweat Glands ◽  
Eccrine Sweat

Sr2+ substitutes for Ca2+ in methacholine (MCH)-evoked sweat secretion in isolated simian eccrine sweat glands, but four to eight times greater concentrations of Sr2+ were required to achieve the same effect as did a given Ca2+ concentration. In Ca2+-free Sr2+ medium the anticholinergic effect of atropine was reduced by about four orders of magnitude. In the Sr2+ medium, spontaneous sweat secretion (SSS) was also observed in the absence of any pharmacological stimuli. SSS occurs slowly, reaching a plateau after 30 min incubation. The maximal SSS is a saturation function of Sr2+ concentration reaching a maximum at 8 mM. Sr2+-induced SSS was inhibitable by removal of Sr2+, low bath temperature (10–14 degrees C), ouabain (5 X 10(-6) M), and D 600 (10(-3) M). Ca2+ was found to inhibit Sr2+-induced SSS, but a Schild plot for the Ca2+ and Sr2+ dose relationship failed to show a slope of unity. The data suggest that Sr2+-induced SSS represents actual secretory processes, which are triggered by Sr2+ leaking into the cell through as yet undefined membrane channels.

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