scholarly journals The contribution of noradrenergic nerves to the vasoconstrictor response during local cooling of leg and forearm skin in humans

2018 ◽  
Vol 37 (01) ◽  
pp. 33-40 ◽  
Author(s):  
Ramzi A. Al-horani ◽  
Mukhallad Mohammad
Keyword(s):  
Local Cooling ◽  
Vasoconstrictor Response ◽  
Noradrenergic Nerves ◽  
Forearm Skin

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.

Oral vitamin C enhances the adrenergic vasoconstrictor response to local cooling in human skin

2012 ◽  
Vol 112 (10) ◽  
pp. 1689-1697 ◽  
Author(s):  
Fumio Yamazaki
Keyword(s):  
Human Skin ◽  
Local Administration ◽  
Adrenergic System ◽  
Local Cooling ◽  
Oral Vitamin ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Forearm Skin ◽  
Cutaneous Vascular Conductance

Local administration of ascorbic acid (Asc) at a supraphysiological concentration inhibits the cutaneous vasoconstrictor response to local cooling (LC). However, whether orally ingesting Asc inhibits the LC-induced vasoconstrictor response remains unknown. The purpose of the present study was to examine the acute influence of oral Asc on the adrenergic vasoconstrictor response to LC in human skin. In experiment 1, skin blood flow (SkBF) was measured by laser-Doppler flowmetry at three sites (forearm, calf, palm). The three skin sites were locally cooled from 34 to 24°C at −1°C/min and maintained at 24°C for 20 min before (Pre) and 1.5 h after (Post) oral Asc (2-g single dose) or placebo supplementation. Cutaneous vascular conductance (CVC) was calculated as the ratio of SkBF to blood pressure and expressed relative to the baseline value before LC. Oral Asc enhanced ( P < 0.05) the reductions in CVC in the forearm (Pre, −50.3 ± 3.3%; Post, −57.8 ± 2.2%), calf (Pre, −52.6 ± 3.7%; Post, −66.1 ± 4.3%), and palm (Pre, −46.2 ± 6.2%; Post, −60.4 ± 5.6%) during LC. The placebo did not change the responses at any site. In experiment 2, to examine whether the increased vasoconstrictor response caused by oral Asc is due to the adrenergic system, the release of neurotransmitters from adrenergic nerves in forearm skin was blocked locally by iontophoresis of bretylium tosylate (BT). Oral Asc enhanced ( P < 0.05) the reductions in CVC at untreated control sites but did not change the responses at BT-treated sites during LC. In experiment 3, to further examine whether adrenergically mediated vasoconstriction is enhanced by oral Asc, 0.1 mM tyramine was administered using intradermal microdialysis in the forearm skin at 34°C in the Pre and Post periods. Oral Asc increased ( P < 0.05) the tyramine-induced reduction in CVC. These findings suggest that oral Asc acutely enhances the cutaneous vasoconstrictor responses to LC through the modification of adrenergic sympathetic mechanisms.

Interactions between local and reflex influences on human forearm skin blood flow

1976 ◽  
Vol 41 (6) ◽  
pp. 826-831 ◽  
Author(s):  
J. M. Johnson ◽  
G. L. Brengelmann ◽  
L. B. Rowell
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Vasoconstrictor Response ◽  
Human Forearm ◽  
Forearm Skin ◽  
Forearm Muscle

A three-part experiment was designed to examine interactions between local and reflex influences on forearm skin blood flow (SkBF). In part I locally increasing arm skin temperature (Tsk) to 42.5 degrees C was not associated with increases in underlying forearm muscle blood flow, esophageal temperature (Tes), or forearm blood flow in the contralateral cool arm. In part II whole-body Tsk was held at 38 or 40 degrees C and the surface temperature of one arm held at 38 or 42 degrees C for prolonged periods. SkBF in the heated arm rose rapidly with the elevation in body Tsk and arm Tsk continued to rise as Tes rose. SkBF in the arm kept at 32 degrees C paralleled rising Tes. In six studies, SkBF in the cool arm ultimately converged with SkBF in the heated arm. In eight other studies, heated arm SkBF maintained an offset above cool arm SkBF throughout the period of whole-body heating. In part III, local arm Tsk of 42.5 degrees C did not abolish skin vasoconstrictor response to lower body negative pressure. We conclude that local and reflex influences to skin interact so as to modify the degree but not the pattern of skin vasomotor response.

Cutaneous and skeletal muscle vascular responses to hypothermia

1981 ◽  
Vol 240 (6) ◽  
pp. H868-H873 ◽  
Author(s):  
T. C. Major ◽  
J. M. Schwinghamer ◽  
S. Winston
Keyword(s):  
Skeletal Muscle ◽  
Vascular Resistance ◽  
Sympathetic Nerves ◽  
Local Cooling ◽  
Right Heart ◽  
Vascular Responses ◽  
External Cooling ◽  
Vasoconstrictor Response ◽  
The Right ◽  
Cutaneous Vasoconstriction

Vascular resistance and capacitance were studied in innervated or denervated canine forelimbs. Hypothermia (38-28 degrees C) was induced systemically, by external cooling of blood which returned to the right heart, or locally, by cooling blood perfusing the forelimb. Systemic cooling to 33 and then to 28 degrees C elicited significant decreases in limb weight with substantial increases in both skin and skeletal muscle vascular resistances. Acute denervation of the forelimbs attenuated both the fall in limb weight and increase in skin vascular resistance associated with cooling. These data support the contention that cutaneous vasoconstriction during systemic cooling is mediated primarily by sympathetic nerves, whereas skeletal muscle vasoconstriction is mediated primarily by circulating hormones. Local cooling elicited skin and skeletal muscle vascular dilation at 33 degrees C in both innervated and denervated forelimbs whereas either no change or a slight increase in skin and skeletal muscle vascular resistance resulted upon local cooling to 28 degrees C, perhaps due to the inhibition of Na+ - K+ - ATPase activity and/or a rise in blood viscosity. The locally induced vasodilation was found to override the powerful vasoconstrictor response caused by systemic cooling. The vasodilation is considered active rather than passive, because the increase in forelimb weight and decreases in forelimb vascular resistances occurred in the denervated as well as innervated limbs.

Rho kinase-mediated local cold-induced cutaneous vasoconstriction is augmented in aged human skin

2007 ◽  
Vol 293 (1) ◽  
pp. H30-H36 ◽  
Author(s):  
Caitlin S. Thompson-Torgerson ◽  
Lacy A. Holowatz ◽  
Nicholas A. Flavahan ◽  
W. Larry Kenney
Keyword(s):  
Rho Kinase ◽  
Age Difference ◽  
Local Cooling ◽  
Kinase Inhibition ◽  
Doppler Flowmetry ◽  
Forearm Skin ◽  
Older Subjects ◽  
Young Subjects ◽  
Effects Of Aging ◽  
Cutaneous Vasoconstriction

Cutaneous vasoconstriction (VC), a critical thermoregulatory response to cold, is generally impaired with aging. However, the effects of aging on local cooling-induced VC and its underlying mechanisms are poorly understood. We tested whether aged skin exhibits attenuated localized cold-induced VC and whether Rho kinase-mediated cold-induced VC is augmented with age. Skin blood flow was monitored with laser Doppler flowmetry (LDF) on seven young and seven older subjects. Cutaneous vascular conductance (CVC; LDF/mean arterial pressure) was expressed as percentage change from baseline (%ΔCVCbase). In protocol 1, two forearm skin sites were cooled to six temperatures (31.5–19°C) for 10 min each or two temperatures (29°C, 24°C) for 30 min each, with no age differences in the magnitude of VC. In protocol 2, three forearm skin sites were instrumented for intradermal microdialysis and cooled to 24°C for 40 min. During minutes 1–5, there was no age difference in CVC responses at control sites (young: −45 ± 6% vs. older: −46 ± 3%, P > 0.9). Adrenoceptor antagonism (yohimbine + propranolol) abolished VC in young (to +15 ± 13%, P < 0.05) but only partially inhibited VC in older subjects (to −23 ± 6%, P < 0.05). Rho kinase inhibition plus adrenoceptor antagonism (yohimbine + propranolol + fasudil) abolished VC in both groups. During minutes 35–40, there was no age difference in control (young: −77 ± 4% vs. older: −70 ± 2%, P > 0.3) or adrenoceptor-antagonized responses (young: −61 ± 3% vs. older: −55 ± 2%, P > 0.3); however, Rho kinase inhibition plus adrenoceptor antagonism blocked more VC in older compared with young subjects (−19 ± 11% vs. −35 ± 3%, P < 0.05). Although its magnitude remains unaffected, cold-induced VC becomes less dependent on adrenergic and more dependent on Rho kinase signaling with advancing age.

The role of baseline in the cutaneous vasoconstrictor responses during combined local and whole body cooling in humans

2007 ◽  
Vol 293 (5) ◽  
pp. H3187-H3192 ◽  
Author(s):  
Gary J. Hodges ◽  
Wojciech A. Kosiba ◽  
Kun Zhao ◽  
Guy E. Alvarez ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Laser Doppler ◽  
Whole Body ◽  
Local Cooling ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Body Cooling ◽  
Whole Body Cooling

Previous work showed that local cooling (LC) attenuates the vasoconstrictor response to whole body cooling (WBC). We tested the extent to which this attenuation was due to the decreased baseline skin blood flow following LC. In eight subjects, skin blood flow was assessed using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was expressed as LDF divided by blood pressure. Subjects were dressed in water-perfused suits to control WBC. Four forearm sites were prepared with microdialysis fibers, local heating/cooling probe holders, and laser-Doppler probes. Three sites were locally cooled from 34 to 28°C, reducing CVC to 45.9 ± 3.9, 42 ± 3.9, and 44.5 ± 4.8% of baseline ( P < 0.05 vs. baseline; P > 0.05 among sites). At two sites, CVC was restored to precooling baseline levels with sodium nitroprusside (SNP) or isoproterenol (Iso), increasing CVC to 106.4 ± 12.4 and 98.9 ± 10.1% of baseline, respectively ( P > 0.05 vs. precooling). Whole body skin temperature, apart from the area of blood flow measurement, was reduced from 34 to 31°C. Relative to the original baseline, CVC decreased ( P < 0.05) by 44.9 ± 2.8 (control), 11.3 ± 2.4 (LC only), 29 ± 3.7 (SNP), and 45.8 ± 8.7% (Iso). The reductions at LC only and SNP sites were less than at control or Iso sites ( P < 0.05); the responses at those latter sites were not different ( P > 0.05), suggesting that the baseline change in CVC with LC is important in the attenuation of reflex vasoconstrictor responses to WBC.

Effects of 14 days of head-down tilt bed rest on cutaneous vasoconstrictor responses in humans

2003 ◽  
Vol 94 (6) ◽  
pp. 2113-2118 ◽  
Author(s):  
Thad E. Wilson ◽  
Manabu Shibasaki ◽  
Jian Cui ◽  
Benjamin D. Levine ◽  
Craig G. Crandall
Keyword(s):  
Bed Rest ◽  
Cycle Ergometer ◽  
Exercise Group ◽  
Lower Limbs ◽  
Response Curves ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Rate Maximum ◽  
Forearm Skin ◽  
Cutaneous Vasoconstriction

This study tested the hypothesis that head-down tilt bed rest (HDBR) reduces adrenergic and nonadrenergic cutaneous vasoconstrictor responsiveness. Additionally, an exercise countermeasure group was included to identify whether exercise during bed rest might counteract any vasoconstrictor deficits that arose during HDBR. Twenty-two subjects underwent 14 days of strict 6° HDBR. Eight of these 22 subjects did not exercise during HDBR, while 14 of these subjects exercised on a supine cycle ergometer for 90 min a day at 75% of pre-bed rest heart rate maximum. To assess α-adrenergic vasoconstrictor responsiveness, intradermal microdialysis was used to locally administer norepinephrine (NE), while forearm skin blood flow (SkBF; laser-Doppler flowmetry) was monitored over microdialysis membranes. Nonlinear regression modeling was used to identify the effective drug concentration that caused 50% of the cutaneous vasoconstrictor response (EC50) and minimum values from the SkBF-NE dose-response curves. In addition, the effects of HDBR on nonadrenergic cutaneous vasoconstriction were assessed via the venoarteriolar response of the forearm and leg. HDBR did not alter EC50 or the magnitude of cutaneous vasoconstriction to exogenous NE administration regardless of whether the subjects exercised during HDBR. Moreover, HDBR did not alter the forearm venoarteriolar response in either the control or exercise groups during HDBR. However, HDBR significantly reduced the magnitude of cutaneous vasoconstriction due to the venoarteriolar response in the leg, and this response was similarly reduced in the exercise group. These data suggest that HDBR does not alter cutaneous vasoconstrictor responses to exogenous NE administration, whereas cutaneous vasoconstriction of the leg due to the venoarteriolar response is reduced after HDBR. It remains unclear whether attenuated venoarteriolar responses in the lower limbs contribute to reduced orthostatic tolerance after bed rest and spaceflight.

Cutaneous vascular responses in finger and forearm during rising ambient temperatures

1960 ◽  
Vol 15 (4) ◽  
pp. 611-618 ◽  
Author(s):  
L. C. Senay ◽  
M. Christensen ◽  
A. B. Hertzman
Keyword(s):  
Skin Temperature ◽  
Heat Exposure ◽  
Local Cooling ◽  
Vascular Events ◽  
Local Skin ◽  
Ambient Temperatures ◽  
Skin Circulation ◽  
Local Skin Temperature ◽  
Forearm Skin ◽  
Additional Influence

During slowly rising ambient temperatures, digital vasodilatation often preceded that in forearm skin; the two vasodilatations proceeded together in spring but not in summer experiments. The curvilinear relation of local skin temperature to local skin blood flow in the forearm often showed an abrupt inflection, suggesting the appearance of an additional influence on the vessels; however, a regular relation to local sweating was not apparent, vasodilatation in forearm skin often continued to increase even when local skin temperature had stabilized or fallen slightly, and the forearm vascular events were prevented by local cooling. During repeat cycles of ambient temperature, complete dissociation of the cutaneous vascular events in finger and forearm and of forearm vasodilatation and sweating often occurred. Digital vasomotor waves were not accompanied by similar waves in forearm skin. Of multiple factors possibly controlling the forearm skin circulation, the local temperature seemed most important. The maximum vasodilatation in forearm during heat exposure was not augmented by acetyl-β-methylcholine. Submitted on January 18, 1960

scholarly journals The involvement of nitric oxide in the cutaneous vasoconstrictor response to local cooling in humans

2006 ◽  
Vol 574 (3) ◽  
pp. 849-857 ◽  
Author(s):  
Gary J. Hodges ◽  
Kun Zhao ◽  
Wojciech A. Kosiba ◽  
John M. Johnson
Keyword(s):  
Nitric Oxide ◽  
Local Cooling ◽  
Vasoconstrictor Response

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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