Acetylcholine released from cholinergic nerves contributes to cutaneous vasodilation during heat stress

2002 ◽  
Vol 93 (6) ◽  
pp. 1947-1951 ◽  
Author(s):  
Manabu Shibasaki ◽  
Thad E. Wilson ◽  
Jian Cui ◽  
Craig G. Crandall
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
No Synthase ◽  
The Other ◽  
Whole Body ◽  
Cholinergic Nerves ◽  
Mean Body Temperature ◽  
Cutaneous Vasodilation ◽  
And Control ◽  
Treated Site

Nitric oxide (NO) contributes to active cutaneous vasodilation during a heat stress in humans. Given that acetylcholine is released from cholinergic nerves during whole body heating, coupled with evidence that acetylcholine causes vasodilation via NO mechanisms, it is possible that release of acetylcholine in the dermal space contributes to cutaneous vasodilation during a heat stress. To test this hypothesis, in seven subjects skin blood flow (SkBF) and sweat rate were simultaneously monitored over three microdialysis membranes placed in the dermal space of dorsal forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine (10 μM), the second membrane was perfused with the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME; 10 mM) dissolved in the aforementioned neostigmine solution (l-NAMENeo), and the third membrane was perfused with Ringer solution as a control site. Each subject was exposed to ∼20 min of whole body heating via a water-perfused suit, which increased mean body temperature from 36.4 ± 0.1 to 37.5 ± 0.1°C ( P < 0.05). After the heat stress, SkBF at each site was normalized to its maximum value, identified by administration of 28 mM sodium nitroprusside. Mean body temperature threshold for cutaneous vasodilation was significantly lower at the neostigmine-treated site relative to the other sites (neostigmine: 36.6 ± 0.1°C, l-NAMENeo: 37.1 ± 0.1°C, control: 36.9 ± 0.1°C), whereas no significant threshold difference was observed between thel-NAMENeo-treated and control sites. At the end of the heat stress, SkBF was not different between the neostigmine-treated and control sites, whereas SkBF at thel-NAMENeo-treated site was significantly lower than the other sites. These results suggest that acetylcholine released from cholinergic nerves is capable of modulating cutaneous vasodilation via NO synthase mechanisms early in the heat stress but not after substantial cutaneous vasodilation.

scholarly journals Roles of nitric oxide synthase isoforms in cutaneous vasodilation induced by local warming of the skin and whole body heat stress in humans

2009 ◽  
Vol 107 (5) ◽  
pp. 1438-1444 ◽  
Author(s):  
Dean L. Kellogg ◽  
Joan L. Zhao ◽  
Yubo Wu
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
No Synthase ◽  
Whole Body ◽  
Doppler Flowmetry ◽  
Vasodilator Response ◽  
Cutaneous Vasodilation ◽  
Forearm Skin ◽  
Whole Body Heat Stress ◽  
Body Heat

Nitric oxide (NO) participates in the cutaneous vasodilation caused by increased local skin temperature (Tloc) and whole body heat stress in humans. In forearm skin, endothelial NO synthase (eNOS) participates in vasodilation due to elevated Tloc and neuronal NO synthase (nNOS) participates in vasodilation due to heat stress. To explore the relative roles and interactions of these isoforms, we examined the effects of a relatively specific eNOS inhibitor, Nω-amino-l-arginine (LNAA), and a specific nNOS inhibitor, Nω-propyl-l-arginine (NPLA), both separately and in combination, on skin blood flow (SkBF) responses to increased Tloc and heat stress in two protocols. In each protocol, SkBF was monitored by laser-Doppler flowmetry (LDF) and mean arterial pressure (MAP) by Finapres. Cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Intradermal microdialysis was used to treat one site with 5 mM LNAA, another with 5 mM NPLA, a third with combined 5 mM LNAA and 5 mM NPLA (Mix), and a fourth site with Ringer only. In protocol 1, Tloc was controlled with combined LDF/local heating units. Tloc was increased from 34°C to 41.5°C to cause local vasodilation. In protocol 2, after a period of normothermia, whole body heat stress was induced (water-perfused suits). At the end of each protocol, all sites were perfused with 58 mM nitroprusside to effect maximal vasodilation for data normalization. In protocol 1, at Tloc = 34°C, CVC did not differ between sites ( P > 0.05). LNAA and Mix attenuated CVC increases at Tloc = 41.5°C to similar extents ( P < 0.05, LNAA or Mix vs. untreated or NPLA). In protocol 2, in normothermia, CVC did not differ between sites ( P > 0.05). During heat stress, NPLA and Mix attenuated CVC increases to similar extents, but no significant attenuation occurred with LNAA ( P < 0.05, NPLA or Mix vs. untreated or LNAA). In forearm skin, eNOS mediates the vasodilator response to increased Tloc and nNOS mediates the vasodilator response to heat stress. The two isoforms do not appear to interact during either response.

Forearm cutaneous vascular and sudomotor responses to whole body passive heat stress in young smokers

2015 ◽  
Vol 309 (1) ◽  
pp. R36-R42 ◽  
Author(s):  
Nicole E. Moyen ◽  
Hannah M. Anderson ◽  
Jenna M. Burchfield ◽  
Matthew A. Tucker ◽  
Melina A. Gonzalez ◽  
...  
Keyword(s):  
Heat Stress ◽  
Sweat Gland ◽  
Sweat Rate ◽  
Whole Body ◽  
Mean Body Temperature ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Local Sweat Rate ◽  
Vasomotor Activity ◽  
Young Smokers

The purpose of this study was to compare smokers and nonsmokers' sudomotor and cutaneous vascular responses to whole body passive heat stress. Nine regularly smoking (SMK: 29 ± 9 yr; 10 ± 6 cigarettes/day) and 13 nonsmoking (N-SMK: 27 ± 8 yr) males were passively heated until core temperature (TC) increased 1.5°C from baseline. Forearm local sweat rate (LSR) via ventilated capsule, sweat gland activation (SGA), sweat gland output (SGO), and cutaneous vasomotor activity via laser-Doppler flowmetry (CVC) were measured as mean body temperature increased (ΔTb) during passive heating using a water-perfused suit. Compared with N-SMK, SMK had a smaller ΔTb at the onset of sweating (0.52 ± 0.19 vs. 0.35 ± 0.14°C, respectively; P = 0.03) and cutaneous vasodilation (0.61 ± 0.21 vs. 0.31 ± 0.12°C, respectively; P < 0.01). Increases in LSR and CVC per °C ΔTb (i.e., sensitivity) were similar in N-SMK and SMK (LSR: 0.63 ± 0.21 vs. 0.60 ± 0.40 Δmg/cm2/min/°C ΔTb, respectively, P = 0.81; CVC: 82.5 ± 46.2 vs. 58.9 ± 23.3 Δ%max/°C ΔTb, respectively; P = 0.19). However, the plateau in LSR during whole body heating was higher in N-SMK vs. SMK (1.00 ± 0.13 vs. 0.79 ± 0.26 mg·cm−2·min−1; P = 0.03), which was likely a result of higher SGO (8.94 ± 3.99 vs. 5.94 ± 3.49 μg·gland−1·min−1, respectively; P = 0.08) and not number of SGA (104 ± 7 vs. 121 ± 9 glands/cm2, respectively; P = 0.58). During whole body passive heat stress, smokers had an earlier onset for forearm sweating and cutaneous vasodilation, but a lower local sweat rate that was likely due to lower sweat output per gland. These data provide insight into local (i.e., forearm) thermoregulatory responses of young smokers during uncompensatory whole body passive heat stress.

Evidence of functional beta-adrenoceptors in the cutaneous vasculature

1997 ◽  
Vol 273 (2) ◽  
pp. H1038-H1043 ◽  
Author(s):  
C. G. Crandall ◽  
R. A. Etzel ◽  
J. M. Johnson
Keyword(s):  
Blood Flow ◽  
Ringer Solution ◽  
The Other ◽  
Whole Body ◽  
Beta Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Cutaneous Vasodilation ◽  
Adrenoceptor Agonist ◽  
Treated Site

During a hyperthermic challenge, skin blood flow (SkBF) increases primarily through activation of the cutaneous active vasodilator system. However, mechanisms through which activation of this system elevates SkBF remain unknown. In this project, we sought to identify whether functional beta-adrenoceptors exist on cutaneous vessels and, if present, whether these receptors play an important role in elevating SkBF during a hyperthermic challenge. In protocol 1, SkBF was assessed over two intradermal microdialysis probes. Initially, both probes were perfused with lactated Ringer solution. Probe A was then perfused with a 200 microM solution of the beta-adrenoceptor agonist isoproterenol while probe B was perfused with a 1.7 mM solution of the beta-adrenoceptor antagonist propranolol. Isoproterenol perfusion significantly increased SkBF from 17.7 +/- 2.4 to 70.8 +/- 13.2 perfusion units (PU; P < 0.05), whereas propranolol perfusion did not significantly affect SkBF (23.4 +/- 6.5 to 27.0 +/- 6.8 PU; P > 0.05). After this period, the solutions perfusing the probes were switched. Isoproterenol did not significantly change SkBF at the propranolol-treated site (27.0 +/- 6.8 to 26.4 +/- 7.5 PU; P < 0.05). In protocol 2, SkBF was assessed over two microdialysis probes during indirect whole body heating. One probe was perfused with Ringer solution while the other probe was perfused with 1.7 mM propranolol. The degree of elevation in SkBF during heat stress at the propranolol-treated site (10.4 +/- 1.5 to 35.8 +/- 3.1 PU) was similar to the elevation in SkBF at the Ringer solution site (11.6 +/- 1.0 to 35.0 +/- 1.2 PU). These data demonstrate the presence of functional beta-adrenoceptors in the skin; however, these receptors play no significant role in mediating cutaneous vasodilation during indirect whole body heating.

scholarly journals Combined facial heating and inhalation of hot air do not alter thermoeffector responses in humans

2015 ◽  
Vol 309 (5) ◽  
pp. R623-R627 ◽  
Author(s):  
Jonathan E. Wingo ◽  
David A. Low ◽  
David M. Keller ◽  
Kenichi Kimura ◽  
Craig G. Crandall
Keyword(s):  
Heat Stress ◽  
Respiratory Tract ◽  
Sweat Rate ◽  
Whole Body ◽  
Facial Skin ◽  
Mean Body Temperature ◽  
Doppler Flowmetry ◽  
Hot Air ◽  
Cutaneous Vasodilation ◽  
The Face

The influence of thermoreceptors in human facial skin on thermoeffector responses is equivocal; furthermore, the presence of thermoreceptors in the respiratory tract and their involvement in thermal homeostasis has not been elucidated. This study tested the hypothesis that hot air directed on the face and inhaled during whole body passive heat stress elicits an earlier onset and greater sensitivity of cutaneous vasodilation and sweating than that directed on an equal skin surface area away from the face. Six men and two women completed two trials separated by ∼1 wk. Participants were passively heated (water-perfused suit; core temperature increase ∼0.9°C) while hot air was directed on either the face or on the lower leg (counterbalanced). Skin blood flux (laser-Doppler flowmetry) and local sweat rate (capacitance hygrometry) were measured at the chest and one forearm. During hot-air heating, local temperatures of the cheek and leg were 38.4 ± 0.8°C and 38.8 ± 0.6°C, respectively ( P = 0.18). Breathing hot air combined with facial heating did not affect mean body temperature onsets ( P = 0.97 and 0.27 for arm and chest sites, respectively) or slopes of cutaneous vasodilation ( P = 0.49 and 0.43 for arm and chest sites, respectively), or the onsets ( P = 0.89 and 0.94 for arm and chest sites, respectively), or slopes of sweating ( P = 0.48 and 0.65 for arm and chest sites, respectively). Based on these findings, respiratory tract thermoreceptors, if present in humans, and selective facial skin heating do not modulate thermoeffector responses during passive heat stress.

Mean body temperature does not modulate eccrine sweat rate during upright tilt

2005 ◽  
Vol 98 (4) ◽  
pp. 1207-1212 ◽  
Author(s):  
Thad E. Wilson ◽  
Jian Cui ◽  
Craig G. Crandall
Keyword(s):  
Heat Stress ◽  
Body Temperature ◽  
Peroneal Nerve ◽  
Sweat Rate ◽  
Control Site ◽  
Body Temperatures ◽  
Mean Body Temperature ◽  
Head Up Tilt ◽  
Treated Site ◽  
Eccrine Sweat

Conflicting reports exist about the role of baroreflexes in efferent control of eccrine sweat rate. These conflicting reports may be due to differing mean body temperatures between studies. The purpose of this project was to test the hypothesis that mean body temperature modulates the effect of head-up tilt on sweat rate and skin sympathetic nerve activity (SSNA). To address this question, mean body temperature (0.9·internal temperature + 0.1·mean skin temperature), SSNA (microneurography of peroneal nerve, n = 8), and sweat rate (from an area innervated by the peroneal nerve and from two forearm sites, one perfused with neostigmine to augment sweating at lower mean body temperatures and the second with the vehicle, n = 12) were measured in 13 subjects during multiple 30° head-up tilts during whole body heating. At the end of the heat stress, mean body temperature (36.8 ± 0.1 to 38.0 ± 0.1°C) and sweat rate at all sites were significantly elevated. No significant correlations were observed between mean body temperature and the change in SSNA during head-up tilt ( r = 0.07; P = 0.62), sweating within the innervated area ( r = 0.06; P = 0.56), sweating at the neostigmine treated site ( r = 0.04; P = 0.69), or sweating at the control site ( r = 0.01; P = 0.94). Also, for each tilt throughout the heat stress, there were no significant differences in sweat rate (final tilt sweat rates were 0.69 ± 0.11 and 0.68 ± 0.11 mg·cm−2·min−1 within the innervated area; 1.04 ± 0.16 and 1.06 ± 0.16 mg·cm−2·min−1 at the neostigmine-treated site; and 0.85 ± 0.15 and 0.85 ± 0.15 mg·cm−2·min−1 at the control site, for supine and tilt, respectively). Hence, these data indicate that mean body temperature does not modulate eccrine sweat rate during baroreceptor unloading induced via 30° head-up tilt.

scholarly journals Heat Stress and Cardiovascular, Hormonal, and Heat Shock Proteins in Humans

2012 ◽  
Vol 47 (2) ◽  
pp. 184-190 ◽  
Author(s):  
Masaki Iguchi ◽  
Andrew E. Littmann ◽  
Shuo-Hsiu Chang ◽  
Lydia A. Wester ◽  
Jane S. Knipper ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Heat Shock ◽  
Body Temperature ◽  
Controlled Trial ◽  
Whole Body ◽  
Cord Injury ◽  
Whole Body Heat Stress ◽  
Body Heat

Context: Conditions such as osteoarthritis, obesity, and spinal cord injury limit the ability of patients to exercise, preventing them from experiencing many well-documented physiologic stressors. Recent evidence indicates that some of these stressors might derive from exercise-induced body temperature increases. Objective: To determine whether whole-body heat stress without exercise triggers cardiovascular, hormonal, and extra-cellular protein responses of exercise. Design: Randomized controlled trial. Setting: University research laboratory. Patients or Other Participants: Twenty-five young, healthy adults (13 men, 12 women; age = 22.1 ± 2.4 years, height = 175.2 ± 11.6 cm, mass = 69.4 ± 14.8 kg, body mass index = 22.6 ± 4.0) volunteered. Intervention(s): Participants sat in a heat stress chamber with heat (73°C) and without heat (26°C) stress for 30 minutes on separate days. We obtained blood samples from a subset of 13 participants (7 men, 6 women) before and after exposure to heat stress. Main Outcome Measure(s): Extracellular heat shock protein (HSP72) and catecholamine plasma concentration, heart rate, blood pressure, and heat perception. Results: After 30 minutes of heat stress, body temperature measured via rectal sensor increased by 0.8°C. Heart rate increased linearly to 131.4 ± 22.4 beats per minute (F6,24 = 186, P &lt; .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F6,24 = 10.1, P &lt; .001) and 5 mm Hg (F6,24 = 5.4, P &lt; .001), respectively. Norepinephrine (F1,12 = 12.1, P = .004) and prolactin (F1,12 = 30.2, P &lt; .001) increased in the plasma (58% and 285%, respectively) (P &lt; .05). The HSP72 (F1,12 = 44.7, P &lt; .001) level increased with heat stress by 48.7% ± 53.9%. No cardiovascular or blood variables showed changes during the control trials (quiet sitting in the heat chamber with no heat stress), resulting in differences between heat and control trials. Conclusions: We found that whole-body heat stress triggers some of the physiologic responses observed with exercise. Future studies are necessary to investigate whether carefully prescribed heat stress constitutes a method to augment or supplement exercise.

scholarly journals Local tetrahydrobiopterin administration augments reflex cutaneous vasodilation through nitric oxide-dependent mechanisms in aged human skin

2012 ◽  
Vol 112 (5) ◽  
pp. 791-797 ◽  
Author(s):  
Anna E. Stanhewicz ◽  
Rebecca S. Bruning ◽  
Caroline J. Smith ◽  
W. Larry Kenney ◽  
Lacy A. Holowatz
Keyword(s):  
Nitric Oxide ◽  
Human Skin ◽  
Oxidant Stress ◽  
Local Heat ◽  
Whole Body ◽  
Mean Body Temperature ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Aged Skin ◽  
Reflex Cutaneous Vasodilation

Functional constitutive nitric oxide synthase (NOS) is required for full expression of reflex cutaneous vasodilation that is attenuated in aged skin. Both the essential cofactor tetrahydrobiopterin (BH4) and adequate substrate concentrations are necessary for the functional synthesis of nitric oxide (NO) through NOS, both of which are reduced in aged vasculature through increased oxidant stress and upregulated arginase, respectively. We hypothesized that acute local BH4 administration or arginase inhibition would similarly augment reflex vasodilation in aged skin during passive whole body heat stress. Four intradermal microdialysis fibers were placed in the forearm skin of 11 young (22 ± 1 yr) and 11 older (73 ± 2 yr) men and women for local infusion of 1) lactated Ringer, 2) 10 mM BH4, 3) 5 mM ( S)-(2-boronoethyl)-l-cysteine + 5 mM Nω-hydroxy-nor-l-arginine to inhibit arginase, and 4) 20 mM NG-nitro-l-arginine methyl ester (l-NAME) to inhibit NOS. Red cell flux was measured at each site by laser-Doppler flowmetry (LDF) as reflex vasodilation was induced. After a 1.0°C rise in oral temperature (Tor), mean body temperature was clamped and 20 mM l-NAME was perfused at each site. Cutaneous vascular conductance was calculated (CVC = LDF/mean arterial pressure) and expressed as a percentage of maximum (%CVCmax; 28 mM sodium nitroprusside and local heat, 43°C). Vasodilation was attenuated at the control site of the older subjects compared with young beginning at a 0.3°C rise in Tor. BH4 and arginase inhibition both increased vasodilation in older (BH4: 55 ± 5%; arginase-inhibited: 47 ± 5% vs. control: 37 ± 3%, both P < 0.01) but not young subjects compared with control (BH4: 51 ± 4%CVCmax; arginase-inhibited: 55 ± 4%CVCmax vs. control: 56 ± 6%CVCmax, both P > 0.05) at a 1°C rise in Tor. With a 1°C rise in Tor, local BH4 increased NO-dependent vasodilation in the older (BH4: 31.8 ± 2.4%CVCmax vs. control: 11.7 ± 2.0%CVCmax, P < 0.001) but not the young (BH4: 23 ± 4%CVCmax vs. control: 21 ± 4%CVCmax, P = 0.718) subject group. Together these data suggest that reduced BH4 contributes to attenuated vasodilation in aged human skin and that BH4 NOS coupling mechanisms may be a potential therapeutic target for increasing skin blood flow during hyperthermia in older humans.

scholarly journals Sympathetic nerve activity and whole body heat stress in humans

2011 ◽  
Vol 111 (5) ◽  
pp. 1329-1334 ◽  
Author(s):  
David A. Low ◽  
David M. Keller ◽  
Jonathan E. Wingo ◽  
R. Matthew Brothers ◽  
Craig G. Crandall
Keyword(s):  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Total Activity ◽  
Whole Body ◽  
Internal Temperature ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Mean Body Temperature ◽  
Arterial Blood

We and others have shown that moderate passive whole body heating (i.e., increased internal temperature ∼0.7°C) increases muscle (MSNA) and skin sympathetic nerve activity (SSNA). It is unknown, however, if MSNA and/or SSNA continue to increase with more severe passive whole body heating or whether these responses plateau following moderate heating. The aim of this investigation was to test the hypothesis that MSNA and SSNA continue to increase from a moderate to a more severe heat stress. Thirteen subjects, dressed in a water-perfused suit, underwent at least one passive heat stress that increased internal temperature ∼1.3°C, while either MSNA ( n = 8) or SSNA ( n = 8) was continuously recorded. Heat stress significantly increased mean skin temperature (Δ∼5°C, P < 0.001), internal temperature (Δ∼1.3°C, P < 0.001), mean body temperature (Δ∼2.0°C, P < 0.001), heart rate (Δ∼40 beats/min, P < 0.001), and cutaneous vascular conductance [Δ∼1.1 arbitrary units (AU)/mmHg, P < 0.001]. Mean arterial blood pressure was well maintained ( P = 0.52). Relative to baseline, MSNA increased midway through heat stress (Δ core temperature 0.63 ± 0.01°C) when expressed as burst frequency (26 ± 14 to 45 ± 16 bursts/min, P = 0.001), burst incidence (39 ± 13 to 48 ± 14 bursts/100 cardiac cyles, P = 0.03), or total activity (317 ± 170 to 489 ± 150 units/min, P = 0.02) and continued to increase until the end of heat stress (burst frequency: 61 ± 15 bursts/min, P = 0.01; burst incidence: 56 ± 11 bursts/100 cardiac cyles, P = 0.04; total activity: 648 ± 158 units/min, P = 0.01) relative to the mid-heating stage. Similarly, SSNA (total activity) increased midway through the heat stress (normothermia; 1,486 ± 472 to mid heat stress 6,467 ± 5,256 units/min, P = 0.03) and continued to increase until the end of heat stress (11,217 ± 6,684 units/min, P = 0.002 vs. mid-heat stress). These results indicate that both MSNA and SSNA continue to increase as internal temperature is elevated above previously reported values.

Sensory nerves and nitric oxide contribute to reflex cutaneous vasodilation in humans

2013 ◽  
Vol 304 (8) ◽  
pp. R651-R656 ◽  
Author(s):  
Brett J. Wong
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Core Temperature ◽  
Sensory Nerve ◽  
Sensory Nerves ◽  
Whole Body ◽  
Oral Temperature ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Reflex Cutaneous Vasodilation

We tested the hypothesis that inhibition of cutaneous sensory nerves would attenuate reflex cutaneous vasodilation in response to an increase in core temperature. Nine subjects were equipped with four microdialysis fibers on the forearm. Two sites were treated with topical anesthetic EMLA cream for 120 min. Sensory nerve inhibition was verified by lack of sensation to a pinprick. Microdialysis fibers were randomly assigned as 1) lactated Ringer (control); 2) 10 mM nitro-l-arginine methyl ester (l-NAME) to inhibit nitric oxide synthase; 3) EMLA + lactated Ringer; and 4) EMLA + l-NAME. Laser-Doppler flowmetry was used as an index of skin blood flow, and blood pressure was measured via brachial auscultation. Subjects wore a water-perfused suit, and oral temperature was monitored as an index of core temperature. The suit was perfused with 50°C water to initiate whole body heat stress to raise oral temperature 0.8°C above baseline. Cutaneous vascular conductance (CVC) was calculated and normalized to maximal vasodilation (%CVCmax). There was no difference in CVC between control and EMLA sites (67 ± 5 vs. 69 ± 6% CVCmax), but the onset of vasodilation was delayed at EMLA compared with control sites. The l-NAME site was significantly attenuated compared with control and EMLA sites (45 ± 5% CVCmax; P < 0.01). Combined EMLA + l-NAME site (25 ± 6% CVCmax) was attenuated compared with control and EMLA ( P < 0.001) and l-NAME only ( P < 0.01). These data suggest cutaneous sensory nerves contribute to reflex cutaneous vasodilation during the early, but not latter, stages of heat stress, and full expression of reflex cutaneous vasodilation requires functional sensory nerves and NOS.

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