scholarly journals Effect of elevated local temperature on cutaneous vasoconstrictor responsiveness in humans

2009 ◽  
Vol 106 (2) ◽  
pp. 571-575 ◽  
Author(s):  
Jonathan E. Wingo ◽  
David A. Low ◽  
David M. Keller ◽  
R. Matthew Brothers ◽  
Manabu Shibasaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Local Heating ◽  
Nonlinear Regression Analysis ◽  
Local Skin ◽  
Vasoconstrictor Response ◽  
Independent Mechanism ◽  
Presynaptic Release ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Vasoconstriction

Cutaneous vascular conductance (CVC) increases in response to local skin heating. Although attenuation of vasoconstrictor responsiveness due to local heating has been demonstrated, the mechanism(s) responsible for this attenuation remains unclear. Nitric oxide has been shown to at least partially contribute to this response, but other mechanisms also may be involved. The purpose of this study was to test the hypothesis that local heating diminishes cutaneous vasoconstrictor responsiveness through a nitric oxide-independent mechanism by altering postsynaptic reactivity to norepinephrine. A follow-up protocol tested the hypothesis that local heating attenuates the presynaptic release of neurotransmitters that cause vasoconstriction, also via non-nitric oxide mechanisms. In protocol I, CVC was assessed in eight subjects during administration of increasing doses of norepinephrine (via intradermal microdialysis) at adjacent sites separately heated to 34°C and 40°C. In protocol II, which was identical to, but separate from, protocol I, CVC was assessed in seven subjects during administration of increasing doses of tyramine, which causes release of neurotransmitters from adrenergic nerves. At each site for both protocols, nitric oxide synthesis was inhibited (via microdialysis administration of NG-nitro-l-arginine methyl ester) and flow was matched (via microdialysis administration of adenosine); therefore, temperature was the only variable that differed between the sites. For both protocols, nonlinear regression analysis revealed no difference ( P > 0.05) in the effective drug concentration causing 50% of the vasoconstrictor response. Minimum CVC [6.3 ± 2.0 and 9.0 ± 4.0% of peak CVC (mean ± SD) for protocol I and 19.3 ± 9.3 and 20.5 ± 11.9% of peak CVC for protocol II at 34°C and 40°C sites, respectively] was not different between sites. Independent of nitric oxide, local skin heating to 40°C does not attenuate adrenergically mediated cutaneous vasoconstriction through pre- or postsynaptic mechanisms.

scholarly journals Oral atorvastatin therapy increases nitric oxide-dependent cutaneous vasodilation in humans by decreasing ascorbate-sensitive oxidants

2011 ◽  
Vol 301 (3) ◽  
pp. R763-R768 ◽  
Author(s):  
Lacy A. Holowatz ◽  
W. Larry Kenney
Keyword(s):  
Nitric Oxide ◽  
Local Heating ◽  
Oxidant Stress ◽  
Microvascular Dysfunction ◽  
Local Skin ◽  
Cutaneous Vasodilation ◽  
Before And After ◽  
Atorvastatin Therapy ◽  
Oxide Synthase ◽  
Cutaneous Vascular Conductance

Elevated low-density lipoproteins (LDL) are associated with cutaneous microvascular dysfunction partially mediated by increased arginase activity, which is decreased following a systemic atorvastatin therapy. We hypothesized that increased ascorbate-sensitive oxidant stress, partially mediated through uncoupled nitric oxide synthase (NOS) induced by upregulated arginase, contributes to cutaneous microvascular dysfunction in hypercholesterolemic (HC) humans. Four microdialysis fibers were placed in the skin of nine HC (LDL = 177 ± 6 mg/dl) men and women before and after 3 mo of a systemic atorvastatin intervention and at baseline in nine normocholesterolemic (NC) (LDL = 95 ± 4 mg/dl) subjects. Sites served as control, NOS inhibited, L-ascorbate, and arginase-inhibited+L-ascorbate. Skin blood flow was measured while local skin heating (42°C) induced NO-dependent vasodilation. After the established plateau in all sites, 20 mM ≪ngname≫ was infused to quantify NO-dependent vasodilation. Data were normalized to maximum cutaneous vascular conductance (CVC) (sodium nitroprusside + 43°C). The plateau in vasodilation during local heating (HC: 78 ± 4 vs. NC: 96 ± 2% CVCmax, P < 0.01) and NO-dependent vasodilation (HC: 40 ± 4 vs. NC: 54 ± 4% CVCmax, P < 0.01) was reduced in the HC group. Acute L-ascorbate alone (91 ± 5% CVCmax, P < 0.001) or combined with arginase inhibition (96 ± 3% CVCmax, P < 0.001) augmented the plateau in vasodilation in the HC group but not the NC group (ascorbate: 96 ± 2; combo: 93 ± 4% CVCmax, both P > 0.05). After the atorvastatin intervention NO-dependent vasodilation was augmented in the HC group (HC postatorvastatin: 64 ± 4% CVCmax, P < 0.01), and there was no further effect of ascorbate alone (58 ± 4% CVCmax, P > 0.05) or combined with arginase inhibition (67 ± 4% CVCmax, P > 0.05). Increased ascorbate-sensitive oxidants contribute to hypercholesteromic associated cutaneous microvascular dysfunction which is partially reversed with atorvastatin therapy.

Does local heating-induced nitric oxide production attenuate vasoconstrictor responsiveness to lower body negative pressure in human skin?

2007 ◽  
Vol 102 (5) ◽  
pp. 1839-1843 ◽  
Author(s):  
David A. Low ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
David M. Keller ◽  
Craig G. Crandall
Keyword(s):  
Nitric Oxide ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Local Heating ◽  
Ringer Solution ◽  
No Production ◽  
Lower Body ◽  
Forearm Skin ◽  
Per Se ◽  
Cutaneous Vascular Conductance

We tested the hypothesis that local heating-induced nitric oxide (NO) production attenuates cutaneous vasoconstrictor responsiveness. Eleven subjects (6 men, 5 women) had four microdialysis membranes placed in forearm skin. Two membranes were perfused with 10 mM of NG-nitro-l-arginine (l-NAME) and two with Ringer solution (control), and all sites were locally heated to 34°C. Subjects then underwent 5 min of 60-mmHg lower body negative pressure (LBNP). Two sites (a control and an l-NAME site) were then heated to 39°C, while the other two sites were heated to 42°C. At the l-NAME sites, skin blood flow was elevated using 0.75–2 mg/ml of adenosine in the perfusate solution (Adn + l-NAME) to a similar level relative to control sites. Subjects then underwent another 5 min of 60-mmHg LBNP. At 34°C, cutaneous vascular conductance (CVC) decreased (Δ) similarly at both control and l-NAME sites during LBNP (Δ7.9 ± 3.0 and Δ3.4 ± 0.8% maximum, respectively; P > 0.05). The reduction in CVC to LBNP was also similar between control and Adn + l-NAME sites at 39°C (control Δ11.4 ± 2.5 vs. Adn + l-NAME Δ7.9 ± 2.0% maximum; P > 0.05) and 42°C (control Δ1.9 ± 2.7 vs. Adn + l-NAME Δ 4.2 ± 2.7% maximum; P > 0.05). However, the decrease in CVC at 42°C, regardless of site, was smaller than at 39°C ( P < 0.05). These results do not support the hypothesis that local heating-induced NO production attenuates cutaneous vasoconstrictor responsiveness during high levels of LBNP. However, elevated local temperature, per se, attenuates cutaneous vasoconstrictor responsiveness to LBNP, presumably through non-nitric oxide mechanisms.

Sympathetic, sensory, and nonneuronal contributions to the cutaneous vasoconstrictor response to local cooling

2005 ◽  
Vol 288 (4) ◽  
pp. H1573-H1579 ◽  
Author(s):  
John M. Johnson ◽  
Tony C. Yen ◽  
Kun Zhao ◽  
Wojciech A. Kosiba
Keyword(s):  
Sensory Nerve ◽  
Sympathetic Nerves ◽  
Local Cooling ◽  
Vascular Responses ◽  
Y1 Receptor ◽  
Vasoconstrictor Response ◽  
Forearm Skin ◽  
Cold Sensitive ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Vasoconstriction

Previous work indicates that sympathetic nerves participate in the vascular responses to direct cooling of the skin in humans. We evaluated this hypothesis further in a four-part series by measuring changes in cutaneous vascular conductance (CVC) from forearm skin locally cooled from 34 to 29°C for 30 min. In part 1, bretylium tosylate reversed the initial vasoconstriction (−14 ± 6.6% control CVC, first 5 min) to one of vasodilation (+19.7 ± 7.7%) but did not affect the response at 30 min (−30.6 ± 9% control, −38.9 ± 6.9% bretylium; both P < 0.05, P > 0.05 between treatments). In part 2, yohimbine and propranolol (YP) also reversed the initial vasoconstriction (−14.3 ± 4.2% control) to vasodilation (+26.3 ± 12.1% YP), without a significant effect on the 30-min response (−26.7 ± 6.1% YP, −43.2 ± 6.5% control; both P < 0.05, P > 0.05 between sites). In part 3, the NPY Y1 receptor antagonist BIBP 3226 had no significant effect on either phase of vasoconstriction ( P > 0.05 between sites both times). In part 4, sensory nerve blockade by anesthetic cream (Emla) also reversed the initial vasoconstriction (−20.1 ± 6.4% control) to one of vasodilation (+213.4 ± 87.0% Emla), whereas the final levels did not differ significantly (−37.7 ± 10.1% control, −37.2 ± 8.7% Emla; both P < 0.05, P > 0.05 between treatments). These results indicate that local cooling causes cold-sensitive afferents to activate sympathetic nerves to release norepinephrine, leading to a local cutaneous vasoconstriction that masks a nonneurogenic vasodilation. Later, a vasoconstriction develops with or without functional sensory or sympathetic nerves.

scholarly journals Endothelial nitric oxide synthase control mechanisms in the cutaneous vasculature of humans in vivo

2008 ◽  
Vol 295 (1) ◽  
pp. H123-H129 ◽  
Author(s):  
Dean L. Kellogg ◽  
Joan L. Zhao ◽  
Yubo Wu
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Local Heating ◽  
Ringer Solution ◽  
Whole Body ◽  
Control Mechanisms ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Whole Body Heat Stress ◽  
Body Heat

Nitric oxide (NO) participates in locally mediated vasodilation induced by increased local skin temperature (Tloc) and in sympathetically mediated vasodilation during whole body heat stress. We hypothesized that endothelial NOS (eNOS) participates in the former, but not the latter, response. We tested this hypothesis by examining the effects of the eNOS antagonist NG-amino-l-arginine (l-NAA) on skin blood flow (SkBF) responses to increased Tloc and whole body heat stress. Microdialysis probes were inserted into forearm skin for drug delivery. One microdialysis site was perfused with l-NAA in Ringer solution and a second site with Ringer solution alone. SkBF [laser-Doppler flowmetry (LDF)] and blood pressure [mean arterial pressure (MAP)] were monitored, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF ÷ MAP). In protocol 1, Tloc was controlled with LDF/local heating units. Tloc initially was held at 34°C and then increased to 41.5°C. In protocol 2, after a normothermic period, whole body heat stress was induced (water-perfused suits). At the end of both protocols, 58 mM sodium nitroprusside was perfused at both microdialysis sites to cause maximal vasodilation for data normalization. In protocol 1, CVC at 34°C Tloc did not differ between l-NAA-treated and untreated sites ( P > 0.05). Local skin warming to 41.5°C Tloc increased CVC at both sites. This response was attenuated at l-NAA-treated sites ( P < 0.05). In protocol 2, during normothermia, CVC did not differ between l-NAA-treated and untreated sites ( P > 0.05). During heat stress, CVC rose to similar levels at l-NAA-treated and untreated sites ( P > 0.05). We conclude that eNOS is predominantly responsible for NO generation in skin during responses to increased Tloc, but not during reflex responses to whole body heat stress.

Reflex control of cutaneous vasoconstrictor system is reset by exogenous female reproductive hormones

1999 ◽  
Vol 87 (1) ◽  
pp. 381-385 ◽  
Author(s):  
Nisha Charkoudian ◽  
John M. Johnson
Keyword(s):  
Contraceptive Use ◽  
Reproductive Hormones ◽  
Doppler Flowmetry ◽  
Oral Contraceptive Use ◽  
Vasoconstrictor Response ◽  
Reflex Control ◽  
Relationship Of ◽  
The Relationship ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Vasoconstriction

To determine whether cardiovascular influences of exogenous female steroid hormones include effects on reflex thermoregulatory control of the adrenergic cutaneous vasoconstrictor system, we conducted ramp decreases in skin temperature (Tsk) in eight women in both high- and low (placebo)-progesterone/estrogen phases of oral contraceptive use. With the use of water-perfused suits, Tsk was held at 36°C for 10 min (to minimize initial vasoconstrictor activity) and was then decreased in a ramp, ∼0.2°C/min for 12–15 min. Subjects rested supine for 30–40 min before each experiment, and the protocol was terminated before the onset of shivering. Skin blood flow was monitored by laser-Doppler flowmetry and arterial pressure by finger photoplethysmography. In all experiments, cutaneous vasoconstriction began immediately with the onset of cooling, and cutaneous vascular conductance (CVC) decreased progressively with decreasing Tsk. Regression analysis of the relationship of CVC to Tsk showed no difference in slope between phases (low-hormone phase: 17.67 ± 5.57; high-hormone phase: 17.40 ± 8.00 %baseline/°C; P > 0.05). Additional studies involving local blockade confirmed this response as being solely due to the adrenergic vasoconstrictor system. Waking oral temperature (Tor) was significantly higher on high-hormone vs. low-hormone days (36.60 ± 0.11 vs. 36.37 ± 0.09 °C, respectively; P < 0.02). Integrative analysis of CVC in terms of simultaneous values for Tsk and Tor showed that the cutaneous vasoconstrictor response was shifted in the high-hormone phase such that a higher Tor was maintained throughout cooling ( P < 0.05). Thus reflex thermoregulatory control of the cutaneous vasoconstrictor system is shifted to higher internal temperatures by exogenous female reproductive hormones.

Cutaneous vasoconstrictor responses to norepinephrine are attenuated in older humans

2005 ◽  
Vol 288 (5) ◽  
pp. R1108-R1113 ◽  
Author(s):  
Caitlin S. Thompson ◽  
Lacy A. Holowatz ◽  
W. Larry Kenney
Keyword(s):  
Confidence Interval ◽  
Local Skin ◽  
Local Skin Temperature ◽  
Aged Skin ◽  
Vascular Beds ◽  
Older Subjects ◽  
Young Subjects ◽  
Skin Blood Vessels ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Vasoconstriction

Cutaneous vasoconstriction (VC) in response to cooling is impaired with human aging. On the basis of previous findings that older humans rely predominantly on norepinephrine (NE) for reflex VC of skin blood vessels, and that the VC effects of NE are blunted with age in many vascular beds, we tested the hypothesis that cutaneous VC responses to exogenous NE are attenuated in aged skin compared with young skin. In 11 young (18–30 yr) and 11 older (62–76 yr) men and women, skin blood flow was monitored at two forearm sites with laser Doppler (LD) flowmetry, while local skin temperature was clamped at 34°C. At one site, five doses of NE (10−10 to 10−2 M) were sequentially infused via intradermal microdialysis while the other site served as control (C; Ringer). Cutaneous vascular conductance (CVC; LD flux/mean arterial pressure) was expressed as percent change from baseline (%ΔCVCbase). At 10−10, 10−8, and 10−6 M NE, older VC responses were attenuated compared with young [10−10: −35 (95% confidence interval: −16, −52) vs. −49 (−40, −58) %ΔCVCbase, P = 0.02; 10−8: −38 (−20, −56) vs. −50 (−40, −61) %ΔCVCbase, P = 0.03; 10−6: −52 (−35, −70) vs. −67 (−60, −74) %ΔCVCbase, P = 0.01]. Older maximal VC responses were also blunted compared with young [−80 (confidence interval: −73,−87) vs. −88 (confidence interval: −87, −90) %ΔCVCbase, P = 0.03]. NE-mediated cutaneous VC is blunted at both physiological and superphysiological doses in older subjects compared with young subjects. Considering that NE is the only functional neurotransmitter mediating reflex VC in aged skin, attenuated NE-mediated VC may further predispose older humans to excess heat loss in the cold.

scholarly journals Passive heat therapy improves cutaneous microvascular function in sedentary humans via improved nitric oxide-dependent dilation

2016 ◽  
Vol 121 (3) ◽  
pp. 716-723 ◽  
Author(s):  
Vienna E. Brunt ◽  
Taylor M. Eymann ◽  
Michael A. Francisco ◽  
Matthew J. Howard ◽  
Christopher T. Minson
Keyword(s):  
Nitric Oxide ◽  
Water Immersion ◽  
Local Heating ◽  
Microvascular Function ◽  
Hot Water ◽  
Heat Therapy ◽  
Before And After ◽  
Synthase Inhibitor ◽  
Doppler Flux ◽  
Cutaneous Vascular Conductance

Passive heat therapy (repeated hot tub or sauna use) reduces cardiovascular risk, but its effects on the mechanisms underlying improvements in microvascular function have yet to be studied. We investigated the effects of heat therapy on microvascular function and whether improvements were related to changes in nitric oxide (NO) bioavailability using cutaneous microdialysis. Eighteen young, sedentary, otherwise healthy subjects participated in 8 wk of heat therapy (hot water immersion to maintain rectal temperature ≥38.5°C for 60 min/session; n = 9) or thermoneutral water immersion (sham, n = 9), and participated in experiments before and after the 8-wk intervention in which forearm cutaneous hyperemia to 39°C local heating was assessed at three microdialysis sites receiving 1) Lactated Ringer's (Control), 2) Nω-nitro-l-arginine (l-NNA; nonspecific NO synthase inhibitor), and 3) 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol), a superoxide dismutase mimetic. The arm used for microdialysis experiments remained out of the water at all times. Data are means ± SE cutaneous vascular conductance (CVC = laser Doppler flux/mean arterial pressure), presented as percent maximal CVC (% CVCmax). Heat therapy increased local heating plateau from 42 ± 6 to 53 ± 6% CVCmax ( P < 0.001) and increased NO-dependent dilation (difference in plateau between Control and l-NNA sites) from 26 ± 6 to 38 ± 4% CVCmax ( P < 0.01), while no changes were observed in the sham group. When data were pooled across all subjects at 0 wk, Tempol had no effect on the local heating response ( P = 0.53 vs. Control). There were no changes at the Tempol site across interventions ( P = 0.58). Passive heat therapy improves cutaneous microvascular function by improving NO-dependent dilation, which may have clinical implications.

Modification of the cutaneous vascular response to exercise by local skin temperature

1984 ◽  
Vol 57 (6) ◽  
pp. 1878-1884 ◽  
Author(s):  
W. F. Taylor ◽  
J. M. Johnson ◽  
D. S. O'Leary ◽  
M. K. Park
Keyword(s):  
Polynomial Regression ◽  
Moderate Intensity ◽  
Base Line ◽  
Local Skin ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Forearm Vascular Conductance ◽  
Leg Exercise ◽  
Response To Exercise ◽  
Cutaneous Vasoconstriction

This study examined how local forearm temperature (Tloc) affects the responsiveness of the cutaneous vasculature to a reflex drive for vasoconstriction. We observed responses in forearm blood flow (FBF) and arterial blood pressure to a 5-min bout of supine leg exercise of moderate intensity (125-175 W) after the forearm had been locally warmed to 36, 38, 40, or 42 degrees C for 48 min. With exercise, FBF fell by 1.82 +/- 0.23, 4.06 +/- 0.58, and 3.64 +/- 1.48 ml X 100 ml-1 X min-1 at 36, 38, and 40 degrees C, respectively, and rose by 2.16 +/- 0.57 ml X 100 ml X min-1 at a Tloc of 42 degrees C (mean +/- SE). Forearm vascular conductance (FVC) fell with the onset of exercise by averages of 2.77 +/- 0.57, 7.02 +/- 0.51, 5.36 +/- 0.85, and 4.17 +/- 0.79 ml X 100 ml-1 X min-1 X 100 mmHg-1 at 36, 38, 40, and 42 degrees C, respectively. Second-order polynomial regression analysis indicated that the reductions in FVC were greatest near a Tloc of 39 degrees C and that at a Tloc of 40 or 42 degrees C the cutaneous vasoconstrictor response to the onset of exercise is attenuated. Although elevated Tloc can be used to increase base-line FBF levels to make cutaneous vasoconstrictor responses more obvious, the direct effects of Tloc on this response must also be considered. We conclude that the optimum Tloc for observing reflex cutaneous vasoconstriction is near 39 degrees C.

Preserved reflex cutaneous vasodilation in cystic fibrosis does not include an enhanced nitric oxide-dependent mechanism

2007 ◽  
Vol 102 (6) ◽  
pp. 2301-2306 ◽  
Author(s):  
Brad W. Wilkins ◽  
Elizabeth A. Martin ◽  
Shelly K. Roberts ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Cystic Fibrosis ◽  
Blood Flow ◽  
Skin Blood Flow ◽  
Local Heating ◽  
No Synthase ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Reflex Cutaneous Vasodilation

In humans, vasoactive intestinal peptide (VIP) may play a role in reflex cutaneous vasodilation during body heating. We tested the hypothesis that the nitric oxide (NO)-dependent contribution to active vasodilation is enhanced in the skin of subjects with cystic fibrosis (CF), compensating for sparse levels of VIP. In 2 parallel protocols, microdialysis fibers were placed in the skin of 11 subjects with CF and 12 controls. Lactated Ringer was perfused at one microdialysis site and NG-nitro-l-arginine methyl ester (2.7 mg/ml) was perfused at a second microdialysis site. Skin blood flow was monitored over each site with laser-Doppler flowmetry. In protocol 1, local skin temperature was increased 0.5°C every 5 s to 42°C, and then it maintained at 42°C for ∼45 min. In protocol 2, subjects wore a tube-lined suit perfused with water at 50°C, sufficient to increase oral temperature (Tor) 0.8°C. Cutaneous vascular conductance (CVC) was calculated (flux/mean arterial pressure) and scaled as percent maximal CVC (sodium nitroprusside; 8.3 mg/ml). Vasodilation to local heating was similar between groups. The change (Δ%CVCmax) in CVC with NO synthase inhibition on the peak (9 ± 3 vs. 12 ± 5%CVCmax; P = 0.6) and the plateau (45 ± 3 vs. 35 ± 5%CVCmax; P = 0.1) phase of the skin blood flow response to local heating was similar in CF subjects and controls, respectively. Reflex cutaneous vasodilation increased CVC in CF subjects (58 ± 4%CVCmax) and controls (53 ± 4%CVCmax; P = 0.37) and NO synthase inhibition attenuated CVC in subjects with CF (37 ± 6%CVCmax) and controls (35 ± 5%CVCmax; P = 0.8) to a similar degree. Thus the preservation of cutaneous active vasodilation in subjects with CF is not associated with an enhanced NO-dependent vasodilation.

Influence of hyperoxia on skin vasomotor control in normothermic and heat-stressed humans

2007 ◽  
Vol 103 (6) ◽  
pp. 2026-2033 ◽  
Author(s):  
Fumio Yamazaki ◽  
Kazuo Takahara ◽  
Ryoko Sone ◽  
John M. Johnson
Keyword(s):  
Thermal Conditions ◽  
Inhibitory Effects ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Forearm Skin ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Cutaneous Vascular Conductance ◽  
Male Subjects ◽  
Cutaneous Vasoconstriction

Hyperoxia induces skin vasoconstriction in humans, but the mechanism is still unclear. In the present study we examined whether the vasoconstrictor response to hyperoxia is through activated adrenergic function ( protocol 1) or through inhibitory effects on nitric oxide synthase (NOS) and/or cyclooxygenase (COX) ( protocol 2). We also tested whether any such vasoconstrictor effect is altered by body heating. In protocol 1 ( n = 11 male subjects), release of norepinephrine from adrenergic terminals in the forearm skin was blocked locally by iontophoresis of bretylium (BT). In protocol 2, the NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME) and the nonselective COX antagonist ketorolac (Keto) were separately administered by intradermal microdialysis in 11 male subjects. In the two protocols, subjects breathed 21% (room air) or 100% O2 in both normothermia and hyperthermia. Skin blood flow (SkBF) was monitored by laser-Doppler flowmetry. Cutaneous vascular conductance (CVC) was calculated as the ratio of SkBF to blood pressure measured by Finapres. In protocol 1, breathing 100% O2 decreased ( P < 0.05) CVC at the BT-treated and at untreated sites from the levels of CVC during 21% O2 breathing both in normothermia and hyperthermia. In protocol 2, the administration of l-NAME inhibited ( P < 0.05) the reduction of CVC during 100% O2 breathing in both thermal conditions. The administration of Keto inhibited ( P < 0.05) the reduction of CVC during 100% O2 breathing in hyperthermia but not in normothermia. These results suggest that skin vasoconstriction with hyperoxia is partly due to the decreased activity of functional NOS in normothermia and hyperthermia. We found no significant role for adrenergic mechanisms in hyperoxic vasoconstriction. Decreased production of vasodilator prostaglandins may play a role in hyperoxia-induced cutaneous vasoconstriction in heat-stressed humans.

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