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PubMed1984

Cyclic GMP accumulation during cholinergic stimulation of eccrine sweat glands.

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.

Animals↗

PubMed1987

Nonisotonicity of simian eccrine primary sweat induced in vitro.

Na+, K+, Cl-, and HCO-3 concentrations were determined in both methacholine (MCh)-induced and isoproterenol (ISO)-induced primary sweat collected directly from isolated and cannulated rhesus monkey palm eccrine secretory coils in vitro. Na+ concentration [( Na+]) of MCh-induced sweat was higher than that of the bathing medium by 4.2 mM, i.e., 155.4 vs. 151.2 mM. Sweat [Cl-] was consistently higher than that of the medium by 13.7 and 11.2 mM in both MCh- and ISO-induced primary fluid, respectively. The sweat-to-bath Cl- gradient increased as [Cl-] in the bath was lowered by substituting with less-permeable anions. In contrast sweat [HCO-3] was much lower in both MCh- and ISO-induced sweat than that of the bathing medium, i.e., approximately 6 mM in sweat vs. 25 mM in the bath. [K+] in MCh-induced primary sweat (mean of 6.63 mM) was consistently higher than that of the bathing medium (5 mM). Furthermore, [K+] tended to be the highest in the first sweat sample after MCh stimulation, reaching as high as 9 mM. In sharp contrast ISO-induced primary sweat showed [K+] that was almost always less than 5 mM with the mean of 4.03 mM. These electrolyte profiles of the primary fluid have been discussed relative to the transport model generally applied for Cl- secretory epithelia.

Animals↗

PubMed1987

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

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.

Animals↗

PubMed1982

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

Biopsy specimens from the chest, palm, back, and lateral calf were obtained from three patas (4-6 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.

Animals↗

PubMed1999

Equine sweating responses to submaximal exercise during 21 days of heat acclimation.

This study examined sweating responses in six exercise-trained horses during 21 consecutive days (4 h/day) of exposure to, and daily exercise in, hot humid conditions (32-34 degrees C, 80-85% relative humidity). On days 0, 3, 7, 14, and 21, horses completed a standardized exercise test on a treadmill (6 degrees incline) at a speed eliciting 50% of maximal O(2) uptake until a pulmonary artery temperature of 41.5 degrees C was attained. Sweat was collected at rest, every 5 min during exercise, and during 1 h of standing recovery for measurement of ion composition (Na(+), K(+), and Cl(-)) and sweating rate (SR). There was no change in the mean time to reach a pulmonary artery temperature of 41.5 degrees C (range 19.09 +/- 1.41 min on day 0 to 20.92 +/- 1.98 min on day 3). Peak SR during exercise (ml. m(-2). min(-1)) increased on day 7 (57.5 +/- 5. 0) but was not different on day 21 (48.0 +/- 4.7) compared with day 0 (52.0 +/- 3.4). Heat acclimation resulted in a 17% decline in SR during recovery and decreases in body mass and sweat fluid losses during the standardized exercise test of 25 and 22%, respectively, by day 21. By day 21, there was also a 10% decrease in mean sweat Na(+) concentration for a given SR during exercise and recovery; this contributed to an approximately 26% decrease in calculated total sweat ion losses (3,112 +/- 114 mmol on day 0 vs. 2,295 +/- 107 mmol on day 21). By day 21, there was a decrease in sweating threshold ( approximately 1 degrees C) but no change in sweat sensitivity. It is concluded that horses responded to 21 days of acclimation to, and exercise in, hot humid conditions with a reduction in sweat ion losses attributed to decreases in sweat Na(+) concentration and SR during recovery.

Acclimatization↗

PubMed1991

Sweat-related dermatoses: old concept and new scenario.

This review focuses on dermatoses that are caused by the presence of sweat--a previously underemphasized subject. A working classification based on 'internal sweating' (extravasated sweat in the dermis and epidermis) and 'external sweating' (sweat on skin surface) is proposed. Clinical observations suggest that transient acantholytic dermatosis is the consequence of extravasated sweat; we speculate that it is an example of sweat-related, protease-induced epidermal acantholysis. Neutrophilic eccrine hidradenitis may represent a sweat-related drug reaction. We emphasize the well-recognized phenomenon of 'sweat retention syndrome' in a new scenario: hospitalized febrile patients, increasing use of chemotherapy, new life style. The concept of 'sweat-gland-mediated cutaneous inflammation' is proposed.

Humans↗

PubMed2005

Sweat production during global heating and during isometric exercise in people with diabetes.

BACKGROUND: While sweat production in response to heat is impaired in people with diabetes, sweat production has not been examined during isometric exercise. MATERIAL/METHODS: Eight subjects with type 2 diabetes and 9 control subjects exerted a fatiguing isometric contraction of the handgrip muscles at a tension of 40% of the maximum voluntary strength (MVC) after exposure to a 32 deg C environment for 30 min. compared to 10 controls and 10 subjects with diabetes exposed to a 39 deg C environment. RESULTS: Sweat was impaired to all areas of the body during heat exposure in patients with diabetes under both environmental conditions. For example, on the chest, the average sweat rates after exposure to the 32 deg environment was 259.2 +/- 55.2 nanoliters/min in control subjects and 198.3 +/- 46.2 nanoliters/min for subjects with diabetes. Compared to the 32 deg C environment, control subjects increased sweat in all 4 areas proportionally more than subjects with diabetes. Sudomotor rhythm was present in sweat in control subjects at a rate of repetition of 11 and 50 seconds but almost absent in subjects with diabetes. During exercise, sweat rates slowly increased from the beginning to the end of the exercise. But the head of the subjects with diabetes showed hypersweating while the other areas showed diminished sweating compared to control subjects. CONCLUSIONS: Thus some of the impairment in sweating may be due to central mechanisms associated with heat sensitivity or in the hypothalamus and not to the sweat glands themselves.

Adult↗

PubMed2005

Sweat-testing in preterm and full-term infants less than 6 weeks of age.

Our objective was to examine the characteristics of preterm and full-term infants < or = 6 weeks old that influence the success of obtaining sufficient sweat for diagnosis of CF, and corresponding sweat chloride concentrations. A retrospective chart review of 119 sweat tests was performed on 103 preterm and full-term infants < or = 6 weeks of age. Bivariate and multivariate regression analyses were used to determine the predictors of successful sweat testing and characteristics influencing sweat chloride concentrations. Adequate amounts of sweat (> or = 75 mg) were obtained for analysis in 73.8% of initial attempts in the infant group. The following characteristics were associated with increased odds of obtaining a quantity not sufficient (QNS) for sweat chloride concentration measurement: African-American race, infant weight < 2,000 g, preterm birth, and postmenstrual age (PMA) < 36 weeks. With a multivariable logistic model, the only significant predictors were African-American race (7.3, 2.4-21.7) and PMA < 36 weeks (17.9, 4.2-75.9). Sweat chloride concentration in non-CF individuals is inversely related to both gestational age and age at testing, and this effect is additive in a linear regression model. In conclusion, sweat collection can be reliably performed in infants > or = 36 weeks postmenstrual age, > 2,000 g, and > 3 days postnatal age. Maturational factors have a mild impact on sweat chloride concentration.

Black or African American↗

PubMed1997

Intense exercise increases the post-exercise threshold for sweating.

We demonstrated previously that esophageal temperature (T(es)) remains elevated by approximately 0.5 degrees C for at least 65 min after intense exercise. Following exercise, average skin temperature (T(avg)) and skin blood flow returned rapidly to pre-exercise values even though T(es) remained elevated, indicating that the T(es) threshold for vasodilation is elevated during this period. The present study evaluates the hypothesis that the threshold for sweating is also increased following intense exercise. Four males and three females were immersed in water (water temperature, T(w) = 42 degrees C) until onset of sweating (Immersion 1), followed by recovery in air (air temperature, T(a) = 24 degrees C). At a T(a) of 24 degrees C, 15 min of cycle ergometry (70% VO2max) (Exercise) was then followed by 30 min of recovery. Subjects were then immersed again (T(w) = 42 degrees C) until onset of sweating (Immersion 2). Baseline T(es) and T(skavg) were 37.0 (0.1) degrees C and 32.3 (0.3) degrees C, respectively. Because the T(skavg) at the onset of sweating was different during Exercise [30.9 (0.3) degrees C] than during Immersion 1 and Immersion 2 [36.8 (0.2) degrees C and 36.4 (0.2) degrees C, respectively] a corrected core temperature, T((es) (calculated)), was calculated at a single designated skin temperature, T((sk)(designated)), as follows: T((es)(calculated)) = T(es) + [beta/(1-beta)][T(skavg)-T((sk)(designated))]. The T((sk)(designated)) was set at 36.5 degrees C (mean of Immersion 1 and Immersion 2 conditions) and beta represents the fractional contribution of T(skavg) to the sweating response (beta for sweating = 0.1). While T((es)(calculated)) at the onset of sweating was significantly lower during exercise [36.7 (0.2) degrees C] than during Immersion 1 [37.1 (0.1) degrees C], the threshold of sweating during Immersion 2 [37.3 (0.1) degrees C] was greater than during both Exercise and Immersion 1 (P < 0.05). We conclude that intense exercise decreases the sweating threshold during exercise itself, but elicits a subsequent short-term increase in the resting sweating threshold.

Adult↗

PubMed1986

Sweat sulfate concentrations are decreased in cystic fibrosis.

We have developed methods to measure inorganic sulfate in small volumes of sweat, and compared sulfate concentrations in sweat samples from CF patients and controls. In contrast to the increases in sweat chloride, sweat sulfate concentrations in 13 CF patients were reduced to 68 +/- 24% of control values (mean +/- SD, n = 25, p less than 0.001). Sulfate concentrations in sweat may depend on sweat rates, but the rates were not significantly different in the two study groups. Since we have observed a positive correlation between sweat sulfate and sweat chloride excretion in non-CF subjects in earlier studies, we suggest that the decreased sulfate in CF sweat may bear directly on the nature of the anion permeability defect present in the ductal epithelium of the CF sweat gland.

Adolescent↗

PubMed2005

The sweating response of elite professional soccer players to training in the heat.

Sweat rate and sweat composition vary extensively between individuals, and quantification of these losses has a role to play in the individualisation of a hydration strategy to optimise training and competitive performance. Data were collected from 26 male professional football (soccer) players during one 90 min pre-season training session. This was the 2nd training session of the day, carried out between 19.30 and 21.00 h when the mean +/- SD environment was 32 +/- 3 degrees C, 20 +/- 5 %rh and WBGT 22 +/- 2 degrees C. Training consisted of interval running and 6-a-side games during which the average heart rate was 136 +/- 7 bpm with a maximum rate of 178 +/- 7 bpm (n = 19). Before and after training all players were weighed nude. During training all players had free access to sports drinks (Gatorade) and mineral water (Solan de Cabras). All drink bottles were weighed before and after training. Players were instructed to drink only from their own bottles and not to spit out any drink. No player urinated during the training session. Sweat was collected by patches from the chest, arm, back, and thigh of a subgroup of 7 players. These remained in place for the first 15 - 30 min of the training session, and sweat was analysed for sodium (Na (+)) and potassium (K (+)) concentration. Body mass loss was 1.23 +/- 0.50 kg (ranging from 0.50 to 2.55 kg), equivalent to dehydration of 1.59 +/- 0.61 % of pre-training body mass. The sweat volume lost was 2193 +/- 365 ml (1672 to 3138 ml), but only 972 +/- 335 ml (239 to 1724 ml) of fluid was consumed. 45 +/- 16 % of the sweat volume loss was replaced, but this ranged from 9 % to 73 %. The Na (+) concentration of the subgroup's sweat was 30.2 +/- 18.8 mmol/l (15.5 to 66.3 mmol/l) and Na (+) losses averaged 67 +/- 37 mmol (26 to 129 mmol). The K (+) concentration of the sweat was 3.58 +/- 0.56 mmol/l (2.96 to 4.50 mmol/l) and K (+) losses averaged 8 +/- 2 mmol (5 to 12 mmol). The drinking employed by these players meant that only 23 +/- 21 % of the sweat Na (+) losses were replaced: This ranged from replacing virtually none (when water was the only drink) to replacing 62 % when the sports drink was consumed. These elite soccer players did not drink sufficient volume to replace their sweat loss. This, however, is in accord with data in the literature from other levels of soccer players and athletes in other events. These measurements allow for an individualisation of the club's hydration strategy.

Adult↗

PubMed2000

A simplified cyclic adenosine monophosphate-mediated sweat rate test for quantitative measure of cystic fibrosis transmembrane regulator (CFTR) function.

OBJECTIVE: Sweat production is stimulated by both cholinergic and beta-adrenergic pathways in the sweat gland secretory coil. beta-Adrenergic pathway-mediated sweating is absent in cystic fibrosis (CF) because cyclic adenosine monophosphate (cAMP)-mediated chloride transport through the cystic fibrosis transmembrane regulator (CFTR) is disrupted. We report the development of a rapid, reproducible, macroscopic, and quantitative methodology to test the hypothesis that beta-adrenergic sweat rate discriminates among 3 different CFTR phenotypes-CF, heterozygote CF carriers, and non-CF. STUDY DESIGN: Intradermal injection of a mixture of 50 micromol/L isoproterenol, 5 mmol/L aminophylline (to potentiate the beta-adrenergic stimulation), and 140 micromol/L atropine (to block potential cholinergic stimulation) in lactated Ringer's solution was performed in duplicate on one forearm. A single injection of 0.5 mmol/L methacholine to stimulate sweat production by the cholinergic pathway was performed on the other forearm. Sweat rate was determined as the amount of sweat collected on filter paper over 20 minutes. RESULTS AND CONCLUSIONS: Median cAMP-mediated sweat rates were 1.45 mg/20 min (CF, n = 29), 2.55 mg/20 min (CF heterozygote carriers, n = 30), and 3.65 mg/20 min (non-CF, n = 30) and were significantly different in all 3 groups (P =.0001, Kruskal-Wallis test). Methacholine-stimulated sweat rates were similar for all 3 groups. The cAMP-mediated sweat rate test may be a useful endpoint for studies of new agents to increase the function of CFTR.

Adolescent↗

PubMed2003

Endoscopic transthoracic sympathectomy for upper limb hyperhidrosis: limited sympathectomy does not reduce postoperative compensatory sweating.

OBJECTIVE: Compensatory sweating is the most common and troublesome complication of thoracodorsal sympathectomy. Whether the magnitude of compensatory sweating is related to the extent of sympathectomy is unclear. We investigated the association between the extent of sympathectomy and the occurrence and severity of compensatory sweating after endoscopic transthoracic sympathectomy for upper limb hyperhidrosis. METHODS: From September 1992 to June 2000, data from patients undergoing thoracoscopic sympathectomy to treat primary upper limb hyperhidrosis in our department were prospectively collected. Routine follow-up with clinical examination was performed at 1, 3, and 6 months for the first postoperative year and every year thereafter. Late follow-up (February 2001) was with a standardized questionnaire by mail or telephone concerning compensatory sweating and patient satisfaction. Associations between the extent of sympathectomy and the occurrence and severity of compensatory sweating were analyzed with logistic regression and adjusted for age, gender, and relevant confounding factors. RESULTS: Two hundred sixty-eight sympathectomies were consecutively performed in 134 patients (99 female, 35 male; mean age, 27.8 +/- 6.7 years). In the 84 patients with palmar hyperhidrosis, eight underwent T1-T2 resection, four T1-T3 resection, eight T2-T3 resection, and 64 T2-T4 resection. In the 43 patients with palmar and axillary hyperhidrosis, eight underwent T1-T5 resection and 35 T2-T5 resection. The seven patients with isolated axillary hyperhidrosis underwent T3-T5 sympathectomy. No deaths occurred; one conversion for bleeding, one permanent Horner's syndrome, and six minor complications did occur. The initial cure rate was 99.2%. The initial satisfaction rate was 97%. The mean follow-up period was 44.3 months (range, 7 to 100 months), and complete follow-up was available in 132 patients (98.5%). Ninety-five patients (71.9%) had compensatory sweating develop. Seventy patients (53%) judged their compensatory sweating to be minor and intermittent, and 25 patients (19%) judged it severe (16% embarrassing, 3% disabling). On univariate and multivariate analysis, the extent of denervation was not associated with the occurrence or the severity of compensatory sweating. The late satisfaction rate was 91.5%. Compensatory sweating and temporary relief/recurrence were equally considered to be the main causes of dissatisfaction. CONCLUSION: Compensatory sweating was the most common long-term complication of thoracodorsal sympathectomy for primary hyperhidrosis. Its incidence and severity were not associated with the extent of sympathectomy.

Adult↗

PubMed2001

Evidence for metaboreceptor stimulation of sweating in normothermic and heat-stressed humans.

1. Isometric handgrip (IHG) exercise increases sweat rate and arterial blood pressure, and both remain elevated during post-exercise ischaemia. The purpose of this study was to identify whether the elevation in arterial blood pressure during post-exercise ischaemia contributes to the increase in sweating. 2. In normothermia and during whole-body heating, 2 min IHG exercise at 40% maximal voluntary contraction, followed by 2 min post-exercise ischaemia, was performed with and without bolus intravenous administration of sodium nitroprusside during the ischaemic period. Sodium nitroprusside was administered to reduce blood pressure during post-exercise ischaemia to pre-exercise levels. Sweat rate was monitored over two microdialysis membranes placed in the dermal space of forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine, while the other was perfused with the vehicle. 3. In normothermia, IHG exercise increased sweat rate at the neostigmine-treated site but not at the control site. Sweat rate remained elevated during post-exercise ischaemia even after mean arterial blood pressure returned to the pre-IHG exercise baseline. Subsequent removal of the ischaemia stimulus returned sweat rate to pre-IHG exercise levels. Sweat rate during post-exercise ischaemia without sodium nitroprusside administration followed a similar pattern. 4. During whole-body heating, IHG exercise increased sweat rate at both neostigmine-treated and untreated sites. Similarly, regardless of whether mean arterial blood pressure remained elevated or was reduced during post-exercise ischaemia, sweat rate remained elevated during the ischaemic period. 5. These results suggest that sweating in non-glabrous skin during post-IHG exercise ischaemia is activated by metaboreflex stimulation and not via baroreceptor loading.

Adult↗

PubMed1999

Nocturnal sweating and temperature in depression.

OBJECTIVE: Patients with depression may have altered thermoregulation, such as high nocturnal core temperatures, decreased daytime sweating and subjective complaints of nocturnal sweating. We sought to compare nocturnal sweating in depressed patients and non-depressed controls, and to assess the impact of REM sleep on sweat rates. METHOD: Nocturnal sweat rate, nocturnal temperature and REM sleep were measured during the night in 9 controls and 8 depressed subjects; 7 depressed patients were assessed during recovery. RESULTS: The nocturnal temperature was significantly higher in depressed patients compared to controls, and decreased significantly with recovery. The nocturnal sweat rates of depressed patients did not differ significantly from those of controls, but decreased significantly with recovery. Analyses of sweat rates before, during and after REM sleep indicated a trend for the entire sample to show a decrease in sweat rates during REM. CONCLUSION: The nocturnal sweating rates in the depressed patients suggest that impaired sweating is not the cause of the high nocturnal temperature commonly found in depressed patients.

Adult↗

PubMed2003

Central command is capable of modulating sweating from non-glabrous human skin.

Isometric handgrip exercise (IHG) increases sweating rate without changing core or skin temperatures. The contribution of central command resulting in increases in sweating rate during IHG is unknown. To investigate this question, seven subjects performed IHG (35 % maximum voluntary contraction (MVC) for 2 min) followed by 2-min of post-exercise ischaemia (PEI), with and without partial neuromuscular blockade (PNB). PNB was performed to augment central command during the IHG bout. These trials were conducted while the subject was normothermic, mildly heated, and moderately heated. On the non-exercising arm, forearm sweating rate was monitored over a microdialysis membrane perfused with neostigmine (acetylcholinesterase inhibitor), and at an adjacent untreated site. In normothermia with PNB, despite reduced force production during IHG (17 +/- 9 versus 157 +/- 13 N; P < 0.001), the elevation in sweating rate at the neostigmine-treated site was greater relative to the control IHG bout (P < 0.05). During subsequent PEI, for the PNB trial mean arterial blood pressure (MAP) and sweating rate returned towards pre-IHG levels, while during the control trial these variables remained elevated. During IHG while mildly heated, the elevation in sweating rate was greater during the PNB trial relative to the control trial. In contrast, during moderate heating sweating increased during IHG for both trials, however the elevation in sweating rate during the PNB trial was not greater than during the control trial. These results suggest that central command is capable of modulating sweating rate in all thermal conditions, however its effect is reduced when body temperatures and/or sweating rate are substantially elevated.

Adult↗

PubMed2005

NKCC1 and NHE1 are abundantly expressed in the basolateral plasma membrane of secretory coil cells in rat, mouse, and human sweat glands.

In isolated sweat glands, bumetanide inhibits sweat secretion. The mRNA encoding bumetanide-sensitive Na(+)-K(+)-Cl(-) cotransporter (NKCC) isoform 1 (NKCC1) has been detected in sweat glands; however, the cellular and subcellular protein localization is unknown. Na(+)/H(+) exchanger (NHE) isoform 1 (NHE1) protein has been localized to both the duct and secretory coil of human sweat duct; however, the NHE1 abundance in the duct was not compared with that in the secretory coil. The aim of this study was to test whether mRNA encoding NKCC1, NKCC2, and Na(+)-coupled acid-base transporters and the corresponding proteins are expressed in rodent sweat glands and, if expressed, to determine the cellular and subcellular localization in rat, mouse, and human eccrine sweat glands. NKCC1 mRNA was demonstrated in rat palmar tissue, including sweat glands, using RT-PCR, whereas NKCC2 mRNA was absent. Also, NHE1 mRNA was demonstrated in rat palmar tissue, whereas NHE2, NHE3, NHE4, electrogenic Na(+)-HCO(3)(-) cotransporter 1 NBCe1, NBCe2, electroneutral Na(+)-HCO(3)(-) cotransporter NBCn1, and Na(+)-dependent Cl(-)/HCO(3)(-) exchanger NCBE mRNA were not detected. The expression of NKCC1 and NHE1 proteins was confirmed in rat palmar skin by immunoblotting, whereas NKCC2, NHE2, and NHE3 proteins were not detected. Immunohistochemistry was performed using sections from rat, mouse, and human palmar tissue. Immunoperoxidase labeling revealed abundant expression of NKCC1 and NHE1 in the basolateral domain of secretory coils of rat, mouse, and human sweat glands and low expression was found in the coiled part of the ducts. In contrast, NKCC1 and NHE1 labeling was absent from rat, mouse, and human epidermis. Immunoelectron microscopy demonstrated abundant NKCC1 and NHE1 labeling of the basolateral plasma membrane of mouse sweat glands, with no labeling of the apical plasma membranes or intracellular structures. The basolateral NKCC1 of the secretory coils of sweat glands would most likely account for the observed bumetanide-sensitive NaCl secretion in the secretory coils, and the basolateral NHE1 is likely to be involved in Na(+)-coupled acid-base transport.

Animals↗

PubMed1987

Hyposecretion of beta-adrenergically induced sweating in cystic fibrosis heterozygotes.

In order to determine if expression of the cystic fibrosis gene can be detected in heterozygotes, we determined sweat responses induced by local stimulation with cholinergic and beta-adrenergic agents for 20 heterozygotes, 19 age- and sex-matched controls, and five subjects with cystic fibrosis. Active sweat glands were counted and sweat droplets were collected in constant bore capillaries and measured optically. Each subject was tested two to six times. The central finding was that the sweat response of carriers was significantly lower than controls to beta-adrenergic stimulation (p = 0.0013, two-tailed t test; p less than 0.02, Mann-Whitney U), while cystic fibrosis homozygotes did not sweat at all. In contrast, the cholinergic sweat responses did not differ between carriers and controls. For both groups the correlation between cholinergic and beta-adrenergic sweating was positive, but a linear regression of beta-adrenergic sweat responses as a function of cholinergic sweat responses yielded slopes that were significantly different for the two groups. The ratio of beta-adrenergic to cholinergic sweating was plotted for each subject; the mean ratio of the carriers was approximately half of the mean for the controls (p = 0.0002 using t test or p less than 0.002 using the Mann-Whitney U). Our results confirm previous studies and provide new evidence that carriers have, on average, a beta-adrenergically stimulated secretory response that is significantly reduced relative to the control response.

Adrenergic beta-Agonists↗