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Hyperthermia increases intravascular adenosine triphosphate (ATP) and is associated with greater hyperthermia‐induced cutaneous vasodilation. Hyperthermia may also increase skin interstitial fluid ATP thereby activating cutaneous vascular smooth muscle cells and sweat glands. We evaluated the hypothesis that whole‐body heating would increase skin interstitial fluid ATP, and this response would be associated with an increase in cutaneous vasodilation and sweating. Nineteen (8 females) young adults underwent whole‐body heating using a water‐perfusion suit to increase core temperature by ~1°C during which time cutaneous vascular conductance (CVC, ratio of laser‐Doppler blood flow to mean arterial pressure) and sweat rate (ventilated capsule technique) were measured at four forearm skin sites to minimize between‐site variations. Dialysate from the skin sites were collected via intradermal microdialysis. Heating increased serum ATP, CVC, and sweat rate (all p ≤ 0.031). However, heating did not modulate dialysate ATP (median, baseline vs. end‐heating: 2.38 vs. 2.70 nmol/ml) (p = 0.068), though the effect size was moderate (Cohen's d = 0.566). While the heating‐induced increase in CVC was not correlated with changes in serum ATP (r = 0.439, p = 0.060), we observed a negative correlation (rs = −0.555, p = 0.017) between dialysate ATP and CVC. We did not observe a significant correlation between the heating‐induced sweating and serum, dialysate, or sweat ATP (rs = 0.091 to −0.322, all p ≥ 0.222). Altogether, we showed that passive heating increases ATP in blood and possibly skin interstitial fluid, with the latter potentially blunting cutaneous vasodilation. However, ATP does not appear to modulate sweating. [ABSTRACT FROM AUTHOR]

Temperature elevation due to global warming increases the risks of dehydration, which can induce heat-related illness. Proper rehydration with appropriate amounts of water and electrolytes is essential to aid body fluid homeostasis. Wearable sweat sensors which can monitor both the sweat rate and sweat electrolyte concentration may be an effective tool for determining appropriate rehydration. Here, we developed a novel potentially wearable sensor that can monitor both the local sweat rate and sweat electrolyte concentration continuously. The new device includes a system with a short microfluidic pathway that guides the sweat appearing on the skin to a small space in the device to form a quantifiable droplet. The sweat rate is assessed from the time for the droplet to appear and droplet volume, while an integrated electric sensor detects the sodium chloride concentration in each sweat droplet. We demonstrated that this new device could record both the flow rates of artificial sweat and its sodium chloride concentration in ranges of human sweating with an accuracy within ±10%. This is equivalent to the accuracy of commercially available sweat rate meters and sweat ion sensors. The present study provides a new perspective for the design of wearable sensors that can continuously monitor sweat rates and sweat electrolyte concentrations for potential application to a healthcare device. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Does short‐term heat acclimation enhance whole‐body evaporative heat loss and augment nitric oxide synthase (NOS)‐dependent cutaneous vasodilatation and NOS‐ and cyclooxygenase (COX)‐dependent sweating, in exercising older men?What is the main finding and its importance?Our preliminary data (n = 8) demonstrated that short‐term heat acclimation improved whole‐body evaporative heat loss, but it did not influence the effects of NOS and/or COX inhibition on cutaneous vasodilatation or sweating in older men during an exercise–heat stress. These outcomes might imply that although short‐term heat acclimation enhances heat dissipation in older men, it does not modulate NOS‐ and COX‐dependent control of cutaneous vasodilatation or sweating on the forearm. Ageing is associated with decrements in whole‐body heat loss (evaporative + dry heat exchange), which might stem from alterations in nitric oxide synthase (NOS)‐ and cyclooxygenase (COX)‐dependent cutaneous vasodilatation and sweating. We evaluated whether short‐term heat acclimation would (i) enhance whole‐body heat loss primarily by increasing evaporative heat loss, and (ii) augment NOS‐dependent cutaneous vasodilatation and NOS‐ and COX‐dependent sweating, in exercising older men. Eight older men [mean (SD) age, 59 (8) years] completed a calorimetry and microdialysis trial before and after 7 days of exercise–heat acclimation. For the calorimetry trials, whole‐body evaporative and dry heat exchange were assessed using direct calorimetry during 30 min bouts of cycling at light, moderate and vigorous metabolic heat productions (150, 200 and 250 W/m2, respectively) in dry heat (40°C, 20% relative humidity). For the microdialysis trials, local cutaneous vascular conductance and sweat rate were assessed during 60 min exercise in the heat (35°C, 20% relative humidity) at four dorsal forearm skin sites treated with lactated Ringer solution (control), NOS inhibitor, COX inhibitor or combined NOS and COX inhibitors, via microdialysis. Evaporative heat loss during moderate (P = 0.036) and vigorous (P = 0.021) exercise increased after acclimation. Inhibition of NOS alone reduced cutaneous vascular conductance to a similar extent before and after acclimation (P < 0.040), whereas separate and combined NOS and COX inhibition had no significant effects on sweating relative to the control site (P = 0.745). Our preliminary results might suggest that short‐term heat acclimation improves evaporative heat loss, but does not significantly modulate the contributions of NOS or COX to cutaneous vasodilatation or sweating on the forearm in older men during an exercise–heat stress. [ABSTRACT FROM AUTHOR]

While human eccrine sweat glands respond to adrenergic agonists, there remains a paucity of information on the factors modulating this response. Thus, we assessed the relative contribution of α‐ and β‐adrenergic sweating during a heat exposure and as a function of individual factors of sex and training status. α‐ and β‐adrenergic sweating was assessed in forty‐eight healthy young men (n = 35) and women (n = 13) including endurance‐trained (n = 12) and untrained men (n = 12) under non–heat exposure (temperate, 25°C; n = 17) and heat exposure (hot, 35°C; n = 48) conditions using transdermal iontophoresis of phenylephrine (α‐adrenergic agonist) and salbutamol (β‐adrenergic agonist) on the ventral forearm, respectively. Adrenergic sweating was also measured after iontophoretic administration of atropine (muscarinic receptor antagonist) or saline (control) to evaluate how changes in muscarinic receptor activity modulate the adrenergic response to a heat exposure (n = 12). α‐ and β‐adrenergic sweating was augmented in hot compared with temperate conditions (both P ≤.014), albeit the relative increase was greater in β (~5.4‐fold)‐ as compared to α (~1.5‐fold)‐adrenergic‐mediated sweating response. However, both α‐ and β‐adrenergic sweating was abolished by atropinization (P =.001). Endurance‐trained men showed an augmentation in α‐ (P =.043) but not β (P =.960)‐adrenergic sweating as compared to untrained men. Finally, a greater α‐ and β‐adrenergic sweating response (both P ≤.001) was measured in habitually active men than in women. We show that heat exposure augments α‐and β‐adrenergic sweating differently via mechanisms associated with altered muscarinic receptor activity. Sex and training status modulate this response. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?β‐Adrenergic receptor activation modulates cutaneous vasodilatation and sweating in young adults. In this study, we assessed whether age‐related differences in β‐adrenergic regulation of these responses exist and whether they differ between men and women.What is the main finding and its importance?We showed that ageing augmented β‐adrenergic cutaneous vasodilatation, although the pattern of response differed between men and women. Ageing had no effect on β‐adrenergic sweating in men or women. Our findings advance our understanding of age‐related changes in the regulation of cutaneous vasodilatation and sweating and provide new directions for research on the significance of enhanced β‐adrenergic cutaneous vasodilatation in older adults. β‐Adrenergic receptor agonists, such as isoprenaline, can induce cutaneous vasodilatation and sweating in young adults. Given that cutaneous vasodilatation and sweating responses to whole‐body heating and to pharmacological agonists, such as acetylcholine, ATP and nicotine, can differ in older adults, we assessed whether ageing also modulates β‐adrenergic cutaneous vasodilatation and sweating and whether responses differ between men and women. In the context of the latter, prior reports showed that the effects of ageing on cutaneous vasodilatation (evoked with ATP and nicotine) and sweating (stimulated by acetylcholine) were sex dependent. Thus, in the present study, we assessed the role of β‐adrenergic receptor activation on forearm cutaneous vasodilatation and sweating in 11 young men (24 ± 4 years of age), 11 young women (23 ± 5 years of age), 11 older men (61 ± 8 years of age) and 11 older women (60 ± 8 years of age). Initially, a high dose (100 µm) of isoprenaline was administered via intradermal microdialysis for 5 min to induce maximal β‐adrenergic sweating. Approximately 60 min after the washout period, three incremental doses of isoprenaline were administered (1, 10 and 100 µm, each for 25 min) to assess dose‐dependent cutaneous vasodilatation. Isoprenaline‐mediated cutaneous vasodilatation was greater in both older men and older women relative to their young counterparts. Augmented cutaneous vasodilatory responses were observed at 1 and 10 µm in women and at 100 µm in men. Isoprenaline‐mediated sweating was unaffected by ageing, regardless of sex. We show that ageing augments β‐adrenergic cutaneous vasodilatation differently in men and women, without influencing β‐adrenergic sweating. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?What is the role of nicotinic receptors in the regulation of normothermic cutaneous blood flow and cutaneous vasodilatation and sweating during whole‐body heating induced following resting in a non‐heat‐stress condition?What is the main finding and its importance?Nicotinic receptors modulated cutaneous vascular tone during rest in a non‐heat‐stress condition and in the early stage of heating, but they had a limited role in mediating cutaneous vasodilatation when core temperature increased >0.4°C. Further, the contribution of nicotinic receptors to sweating was negligible during whole‐body heating. Our findings provide new insights into the role of nicotinic receptors in end‐organ function of skin vasculature and sweat glands in humans. Nicotinic receptors are present in human skin including cutaneous vessels and eccrine sweat glands as well as peripheral nerves. We tested the hypothesis that nicotinic receptors do not contribute to the control of cutaneous vascular tone in the normothermic state, but are involved in mediating cutaneous vasodilatation and sweating during a whole‐body passive heat stress in humans. We first performed a nicotinic receptor blocker verification protocol in six young adults (one female) wherein increases in cutaneous vascular conductance and sweating elicited by 10 mm nicotine were blocked by administration of 500 µm hexamethonium to confirm effective blockade. Thereafter, 12 young males participated in a passive heating protocol. After an instrumentation period in a non‐heat‐stress condition, participants rested for a 10 min baseline period. Thereafter, oesophageal temperature was increased by 1.0°C using water‐perfusion suits. Cutaneous vascular conductance, sweat rate, active sweat gland density and sweat output per individual gland were assessed with and without 500 µm hexamethonium administered via intradermal microdialysis. Hexamethonium reduced cutaneous vascular conductance by 22–34% during normothermia and the early stage of heating. However, this effect was diminished as oesophageal temperature increased >0.4°C. Active sweat gland density was reduced by hexamethonium when oesophageal temperature was elevated by 0.4–0.6°C above baseline resting. However, this was paralleled by a marginal increase in sweat gland output. Consequently, sweat rate remained unchanged. We showed that nicotinic receptors modulate cutaneous perfusion during normothermia and the early stage of heating, but not when core temperature increases >0.4°C. Additionally, they play a limited role in mediating sweating during heating. [ABSTRACT FROM AUTHOR]

Purpose: This study investigated the influence of β-adrenergic receptor blockade on sweating during bilateral static knee extension (KE) and lateral isometric handgrip (IH) exercises followed by post-exercise muscle ischemia (PEMI) in habitually trained individuals.Method: Ten habitually trained men (maximum oxygen uptake, 57.1 ± 3.4 ml kg-1 min-1) were mildly heated by increasing their skin temperature, and bilateral KE or lateral IH exercises at an intensity of 60% maximum voluntary contraction were subsequently performed for 1 min, followed by PEMI to stimulate muscle metaboreceptors for 2 min. Sweat rates were measured on the bilateral forearms (KE) or thighs (IH) transdermally administered with 1% propranolol (propranolol, a non-selective β-adrenergic receptor inhibitor) or saline (control) via iontophoresis.Results: Relative to the pre-exercise baseline values, IH exercise (P = 0.038) followed by PEMI (P = 0.041) similarly increased sweat rates on the thighs at both control and propranolol sites (baseline, 0.05 ± 0.04 vs. 0.05 ± 0.04; IH, 0.14 ± 0.12 vs. 0.15 ± 0.14; PEMI, 0.14 ± 0.16 vs. 0.14 ± 0.16 mg cm-2 min-1). KE increased sweat rates on the forearms (P = 0.001) at both control and propranolol sites similarly (baseline, 0.02 ± 0.03 vs. 0.02 ± 0.03; KE, 0.21 ± 0.19 vs. 0.20 ± 0.18), whereas PEMI did not significantly induce sweating at these sites (P = 0.260) (0.09 ± 0.12 and 0.10 ± 0.12 mg cm-2 min-1, respectively).Conclusion: These results suggest that non-thermal drives induced by static exercise and PEMI do not elicit β-adrenergic sweating in habitually trained individuals even when the non-thermal drives are originated from leg(s) under the conditions in the present study. [ABSTRACT FROM AUTHOR]

Purpose: We investigated the influence of inorganic nitrate ([Formula: see text]) supplementation on local sweating and cutaneous vascular responses during exercise in hot conditions.Method: Eight healthy, young subjects were assigned in a randomized, double-blind, crossover design to receive [Formula: see text]-rich beetroot (BR) juice (140 mL/day, containing ~ 8 mmol of [Formula: see text]) and [Formula: see text]-depleted placebo (PL) juice (140 mL/day, containing ~ 0.003 mmol of [Formula: see text]) for 3 days. On day 3 of supplementation, subjects cycled at an intensity corresponding to 55% of [Formula: see text]O2max for 30 min in hot conditions (30 °C, 50% relative humidity). Chest and forearm sweat rate (SR) and skin blood flow (SkBF), were measured continuously. Cutaneous vascular conductance (CVC) was calculated by SkBF/mean arterial pressure (MAP).Results: Prior to exercise, plasma [Formula: see text] (21 ± 6 and 581 ± 161 µM) and nitrite ([Formula: see text], 87 ± 28 and 336 ± 156 nM) concentrations were higher after BR compared to PL supplementation (P ≤ 0.011, n = 6). Oesophageal, mean skin, and mean body temperatures during exercise were not different between conditions. In addition, BR supplementation did not affect SR, SkBF, and CVC during exercise. A lower MAP was found after 30 min of exercise following BR supplementation (112 ± 6 and 103 ± 6 mmHg for PL and BR, respectively, P = 0.021).Conclusion: These results suggest that inorganic [Formula: see text] supplementation, which increases the potential for O2-independent NO production, does not affect local sweating and cutaneous vascular responses, but attenuates blood pressure in young healthy subjects exercising in a hot environment. [ABSTRACT FROM AUTHOR]

The aim of our study was to determine if habitual endurance training can influence the relative contribution of nitric oxide synthase ( NOS) and cyclooxygenase ( COX) in the regulation of sweating during a passive heat stress in young adults. Ten trained athletes and nine untrained counterparts were passively heated until oral temperature (as estimated by sublingual temperature, Tor) increased by 1.5°C above baseline resting. Forearm sweat rate (ventilated capsule) was measured at three skin sites continuously perfused with either lactated Ringer's solution (Control), 10 mmol/L N G-nitro-L-arginine methyl ester (L- NAME, non-selective NOS inhibitor), or 10 mmol/L ketorolac (Ketorolac, non-selective COX inhibitor) via intradermal microdialysis. Sweat rate was averaged for each 0.3°C increase in Tor. Sweat rate at the L- NAME site was lower than Control following a 0.9 and 1.2°C increase in Tor in both groups (all P ≤ 0.05). Relative to the Control site, NOS-inhibition reduced sweating similarly between the groups ( P = 0.51). Sweat rate at the Ketorolac site was not different from the Control at any levels of Tor in both groups ( P > 0.05). Nevertheless, a greater sweat rate was measured at the end of heating in the trained as compared to the untrained individuals ( P ≤ 0.05). We show that NOS contributes similarly to sweating in both trained and untrained individuals during a passive heat stress. Further, no effect of COX on sweating was measured for either group. The greater sweat production observed in endurance-trained athletes is likely mediated by factors other than NOS- and COX-dependent mechanisms. [ABSTRACT FROM AUTHOR]

Purpose: It is recently reported that determining sweat rate (SR) threshold for increasing galvanic skin conductance (GSC) would represent a maximum rate of sweat ion reabsorption in sweat glands. We evaluate the maximum rate of sweat ion reabsorption over skin regions, sex, and long-term exercise training by using the threshold analysis in the present study.Methods: Ten males (2 untrained, 4 sprinters, and 4 distance runners) and 12 females (5 untrained, 4 sprinters, and 3 distance runners) conducted graded cycling exercise for 45 min at low, middle, and high exercise intensities (heart rate 100-110, 120-130, and 140-150 beats/min, respectively) for 10, 15, and 20 min, respectively, at 30 °C and 50% relative humidity. Comparisons were made between males and females and among untrained individuals, distance runners, and sprinters on the back and forearm.Results: SR threshold for increasing GSC on back was significantly higher than that of forearm (P < 0.05) without any sex differences (back 0.70 ± 0.08 and 0.61 ± 0.04, forearm 0.40 ± 0.05 and 0.45 ± 0.06 mg/cm2/min for males and females, respectively). Distance runners and sprinters showed higher SR threshold for increasing GSC than that of untrained subjects on back (P < 0.05) but not on forearm (back 0.45 ± 0.06, 0.83 ± 0.06, and 0.70 ± 0.04, forearm 0.33 ± 0.04, 0.49 ± 0.02, and 0.39 ± 0.07 mg/cm2/min for untrained subjects, distance runners, and sprinters, respectively).Conclusion: These results suggest that the maximum sweat ion reabsorption rate on the back is higher than that of forearm without sex differences. Furthermore, exercise training in distance runners and sprinters improves the maximum sweat ion reabsorption rate on the back. [ABSTRACT FROM AUTHOR]

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Purpose: The purpose of the present study was to develop and describe a simple method to evaluate the rate of ion reabsorption of eccrine sweat glands in human using the measurement of galvanic skin conductance (GSC) and local sweating rate (SR). This purpose was investigated by comparing the SR threshold for increasing GSC with following two criteria of sweat ion reabsorption in earlier studies such as (1) the SR threshold for increasing sweat ion was at approximately 0.2–0.5 mg/cm2/min and (2) exercise heat acclimation improved the sweat ion reabsorption ability and would increase the criteria 1.Methods: Seven healthy non-heat-acclimated male subjects received passive heat treatment both before and after 7 days of cycling in hot conditions (50% maximum oxygen uptake, 60 min/day, ambient temperature 32 °C, and 50% relative humidity).Results: Subjects became partially heat-acclimated, as evidenced by the decreased end-exercise heart rate (p < 0.01), rate of perceived exhaustion (p < 0.01), and oesophageal temperature (p = 0.07), without alterations in whole body sweat loss, from the first to the last day of training. As hypothesized, we confirmed that the SR threshold for increasing GSC was near the predicted SR during passive heating before exercise heat acclimation, and increased significantly after training (0.19 ± 0.09–0.32 ± 0.10 mg/cm2/min, p < 0.05).Conclusions: The reproducibility of sweat ion reabsorption by the eccrine glands in the present study suggests that the relationship between GSC and SR can serve as a new index for assessing the maximum rate of sweat ion reabsorption of eccrine sweat glands in humans. [ABSTRACT FROM AUTHOR]

The purpose of this study was to compare sweating function in sprinters who have trained for several years with untrained subjects and trained endurance runners. Two separate experiments were conducted. Nine sprinters, eight untrained men, and nine distance runners ( $$\dot{V}{\text{o}}_{{ 2 {\text{max}}}}$$ 50.9 ± 1.4, 38.2 ± 1.8, and 59.1 ± 1.2 mL/kg/min, respectively; P < 0.05) were passively heated for 50 min (Experiment 1), and ten sprinters, 11 untrained men and nine distance runners (similar $$\dot{V}{\text{o}}_{{ 2 {\text{max}}}}$$ levels compared with Experiment 1 in each group) had their sweat gland capacity assessed based on acetylcholine-induced sweating rate (SR) (Experiment 2). The slope of the mean non-glabrous SR plotted against change in mean body temperature during passive heating did not differ significantly between sprinters and untrained men (1.21 ± 0.10 and 0.97 ± 0.12 mg cm/min/°C, respectively); in contrast, compared with untrained men, distance runners exhibited a significantly greater slope (1.42 ± 0.11 mg cm/min/°C, P < 0.05). The mean body temperature threshold for SR was not significantly different among the groups. Acetylcholine-induced SR did not differ significantly between sprinters and untrained men, whereas distance runners showed a significantly higher induced SR compared with untrained men. The sweating function was not improved in sprinters who have trained 2-3 h/day, 5 days/week, for at least 3 years compared with untrained men, although the $$\dot{V}{\text{o}}_{{ 2 {\text{max}}}}$$ was markedly greater in sprinters. Thus, there is a case that daily training was not sufficient to improve sweating function in sprinters relative to those in distance runners. [ABSTRACT FROM AUTHOR]

Iontophoretic transdermal administration of N G-nitro- l -arginine methyl ester hydrochloride [ l -NAME, a nitric oxide synthase (NOS) inhibitor] has been used as a non-invasive evaluation of NOS-dependent mechanisms in human skin. However, the availability has yet to be investigated in sweating research. Prior observations using invasive techniques (e.g., intradermal microdialysis technique) to administer l -NAME have implicated that NOS reduces sweating induced by heat stress but rarely influences the response induced by the administration of cholinergic muscarinic receptor agonists. Therefore, we investigated whether the transdermal iontophoretic administration of l -NAME modulates sweating similar to those prior observations. Twenty young healthy adults (10 males, 10 females) participated in two experimental protocols on separate days. Before each protocol, saline (control) and 1% l -NAME were bilaterally administered to the forearm skin via transdermal iontophoresis. In protocol 1, 0.001% and 1% pilocarpine were iontophoretically administered at l -NAME-treated and untreated sites. In protocol 2, passive heating was applied by immersing the lower limbs in hot water (43 °C) until the rectal temperature increased by 0.8 °C above baseline. The sweat rate was continuously measured throughout both protocols. Pilocarpine-induced sweat rate was not significantly different between the control and l -NAME-treated sites in both pilocarpine concentrations (P ≥ 0.316 for the treatment effect and interaction of treatment and pilocarpine concentration). The sweat rate during passive heating was attenuated at the l -NAME-treated site relative to the control (treatment effect, P = 0.020). Notably, these observations are consistent with prior sweating studies administrating l -NAME into human skin using intradermal microdialysis techniques. Based on the similarity of our results with already known observations, we conclude that transdermal iontophoresis of l -NAME is a valid non-invasive technique for the investigation of the mechanisms of sweating related to NOS during heat stress. • A non-invasive method to assess nitric oxide-dependent sweating is required. • Efficacy of transdermal l -NAME iontophoresis on sweating was assessed. • l -NAME iontophoresis could replicate sweat responses consistent with prior studies. • l -NAME iontophoresis is likely a valid method available in sweating research. [ABSTRACT FROM AUTHOR]

Transient receptor potential vanilloid 4 (TRPV4) channels exist in the endothelial cells of cutaneous blood vessels and the secretory cells of eccrine sweat glands. We assessed if exogenous TRPV4 channel activation elicits cutaneous vasodilatation and sweating in humans in vivo, and if so, whether this response is mediated by nitric oxide synthase (NOS)- cyclooxygenase (COX)- and/or Ca2+-sensitive K+ (KCa) channel-related mechanisms. In ten healthy young adults (24±2 years, 5 women), cutaneous vascular conductance and sweat rate were assessed at four dorsal forearm skin sites continuously treated with either: 1) lactated Ringer's solution (Control), 2) 20 mM L-NAME, a non-selective NOS inhibitor, 3) 10 mM ketorolac, a non-selective COX inhibitor, or 4) 50 mM TEA, a non-selective KCa channel blocker. A potent and selective TRPV4 channel agonist, GSK1016790 A (GSK101), was administered to each skin site in a dose-dependent manner (1, 10, 100, 1000 μM each for ≥30min) via intradermal microdialysis. Administration of 100 and 1000 μM GSK101 increased cutaneous vascular conductance from pre-infusion level at the Control site (48±12 and 57±9%max, respectively, P≤0.004). This response was markedly (53–83%) attenuated by NOS inhibition, COX inhibition, or KCa channel blockade (all P≤0.037), except KCa channel blockade had no effect during 1000 μM GSK101 administration. GSK101 did not influence sweat rate regardless of skin site. We showed that in human skin in vivo, exogenous activation of TRPV4 channels mediates cutaneous vasodilatation, but not sweating through NOS, COX, and KCa channel mechanisms. [ABSTRACT FROM AUTHOR]

Galanin receptor subtypes GAL 1 , GAL 2 , and GAL 3 are involved in several biological functions. We hypothesized that 1) GAL 3 receptor activation contributes to sweating but limits cutaneous vasodilation induced by whole-body and local heating without a contribution of GAL 2 ; and 2) GAL 1 receptor activation attenuates both sweating and cutaneous vasodilation during whole-body heating. Young adults underwent whole-body (n = 12, 6 females) and local (n = 10, 4 females) heating. Forearm sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC; ratio of laser-Doppler blood flow to mean arterial pressure) were assessed during whole-body heating (water-perfusion suit circulated with warm (35 °C) water), while CVC was also assessed by local forearm heating (from 33 °C to 39 °C and elevated to 42 °C thereafter; each level of heating maintained for ∼30 min). Sweat rate and CVC were evaluated at four intradermal microdialysis forearm sites treated with either 1) 5% dimethyl sulfoxide (control), 2) M40, a non-selective GAL 1 and GAL 2 receptor antagonist, 3) M871 to selectively antagonize GAL 2 receptor, or 4) SNAP398299 to selectively antagonize GAL 3 receptor. Sweating was not modulated by any GAL receptor antagonist (P > 0.169), whereas only M40 reduced CVC (P ≤ 0.003) relative to control during whole-body heating. Relative to control, SNAP398299 augmented the initial and sustained increase in CVC during local heating to 39 °C, and the transient increase at 42 °C (P ≤ 0.028). We confirmed that while none of the galanin receptors modulate sweating during whole-body heating, GAL 1 receptors mediate cutaneous vasodilation. Further, GAL 3 receptors blunt cutaneous vasodilation during local heating. [ABSTRACT FROM AUTHOR]