No direct role for <scp>A</scp>1/<scp>A</scp>2 adenosine receptor activation to reflex cutaneous vasodilatation during whole‐body heat stress in humans

Fieger, Sarah M.; Wong, Brett J.

doi:10.1111/j.1748-1716.2012.02426.x

Cited by 18 publications

(28 citation statements)

References 36 publications

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“…As Cheng et al (1996) demonstrated a tone-dependent effect of adenosine on vessel opening, it is not unreasonable to propose that the different baseline thermal status (i.e. following cooling in the present study, and from normothermia in the study by Fieger & Wong, 2012) contributed to the slight differences in findings. Further research is warranted to examine this possibility, because no tone-dependent effects have been demonstrated in human skin.…”

Section: Adenosine and Cutaneous Vasodilatationcontrasting

confidence: 42%

“…The theophylline concentration used was based on that reported by Fieger & Wong (2010, 2012, while that for L-NAME was chosen based on previous studies (Minson et al 2001;Fieger & Wong, 2010). Infusions were maintained for a 45 min period to ensure the establishment of each blockade (Minson et al 2001;Fieger & Wong, 2010).…”

Section: Experimental Designmentioning

confidence: 99%

“…Although the role of adenosine has been examined in other tissues of the human body, there is relatively little known about its influence on cutaneous blood flow. Recent studies have examined the contribution of adenosine to vasodilatation induced by local (Fieger & Wong, 2010) and whole-body heating (Fieger & Wong, 2012). Although these studies showed a contribution of adenosine during local heating, no direct contribution was observed during whole-body heating.…”

Section: Introductionmentioning

confidence: 99%

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Adenosine receptor inhibition attenuates the decrease in cutaneous vascular conductance during whole‐body cooling from hyperthermia

Swift

McGinn

Gagnon

et al. 2013

Experimental Physiology

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New Findings r What is the central question of this study?Adenosine has been implicated in mediating both vasoconstriction and vasodilatation in a variety of tissues throughout the body. No study has yet examined its influence in cutaneous vasoconstriction elicited by whole-body cooling from normothermia or from hyperthermia. r What is the main finding and its importance?Through the use of the non-selective adenosine receptor antagonist, theophylline, a role for adenosine in the control of the cutaneous circulation when cooling from a state of hyperthermia is suggested.Adenosine has both vasodilatory and vasoconstrictive properties, yet its influence on cutaneous vascular conductance (CVC) during whole-body cooling remains unknown. The present study evaluated the influence of adenosine on reflex cutaneous vasoconstriction. Four microdialysis probes were inserted into the dorsal forearm skin of eight subjects and infused with the following solutions: (i) lactated Ringer solution (CON); (ii) 4 mm theophylline (Theo), a non-selective adenosine receptor antagonist; (iii) 10 mm l-NAME, an inhibitor of nitric oxide synthase; and (iv) combined 4 mm theophylline and 10 mm l-NAME (Theo + l-NAME). Subjects subsequently donned a water-perfusion garment. Following a thermoneutral baseline period, the suit was perfused with water at 10• C for 20 min (Cooling 1). The suit was then perfused with water at 49• C for 45 min (Heating), followed by a second cooling period of 20 min using 10 • C water (Cooling 2). Cutaneous blood flow (laser-Doppler) was measured over each microdialysis probe and used to calculate CVC as a percentage of the maximum determined by sodium nitroprusside infusion and local heating. Cutaneous vascular conductance was significantly elevated at the Theo site relative to CON following Cooling 1 (18 ± 6 versus 8 ± 2%; P = 0.01) and Cooling 2 (27 ± 11 versus 14 ± 5%; P = 0.022). Likewise, CVC at the Theo + l-NAME site remained greater compared with l-NAME after Cooling 1 (13 ± 4 versus 7 ± 3%; P = 0.030) and Cooling 2 (15 ± 3 versus 9 ± 2%; P = 0.009). The present findings demonstrate that non-selective antagonism of adenosine receptors attenuates the decrease in cutaneous vascular conductance during wholebody cooling from hyperthermia.

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Section: Adenosine and Cutaneous Vasodilatationcontrasting

confidence: 42%

Section: Experimental Designmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Adenosine receptor inhibition attenuates the decrease in cutaneous vascular conductance during whole‐body cooling from hyperthermia

Swift

McGinn

Gagnon

et al. 2013

Experimental Physiology

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“…Maximal cutaneous vasodilation was elicited via infusion of sodium nitroprusside (SNP) at a rate of 2 l/min and increasing the temperature of the local heating units to 43°C. This temperature increase and dose of SNP have been previously determined effective in eliciting a maximal skin blood flow response (6,7,11,(27)(28)(29).…”

Section: Ethical Approval the Institutional Review Board At Kansas Smentioning

confidence: 98%

“…We, and others, have previously shown a 10 mM concentration of L-NAME adequately inhibits NOS in human skin (6,7,11,20,21,(27)(28)(29), and this duration of EMLA cream inhibits sensory nerve function (10,21,22). All drug treatments were dissolved in lactated Ringer (Baxter Healthcare; Deerfield, IL) and were perfused at a constant rate of 2 l/min with a microinfusion pump (Bee Hive controller and Baby Bee Syringe Pumps; Bioanalytical Systems, West Lafayette, IN).…”

Section: Ethical Approval the Institutional Review Board At Kansas Smentioning

confidence: 99%

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

Wong

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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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 (%CVC(max)). There was no difference in CVC between control and EMLA sites (67 ± 5 vs. 69 ± 6% CVC(max)), 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% CVC(max); P < 0.01). Combined EMLA + L-NAME site (25 ± 6% CVC(max)) 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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Cutaneous Vasodilator and Vasoconstrictor Mechanisms in Temperature Regulation

Johnson

Minson

Kellogg

2014

Comprehensive Physiology

338

290

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In this review, we focus on significant developments in our understanding of the mechanisms that control the cutaneous vasculature in humans, with emphasis on the literature of the last half-century. To provide a background for subsequent sections, we review methods of measurement and techniques of importance in elucidating control mechanisms for studying skin blood flow. In addition, the anatomy of the skin relevant to its thermoregulatory function is outlined. The mechanisms by which sympathetic nerves mediate cutaneous active vasodilation during whole body heating and cutaneous vasoconstriction during whole body cooling are reviewed, including discussions of mechanisms involving cotransmission, NO, and other effectors. Current concepts for the mechanisms that effect local cutaneous vascular responses to local skin warming and cooling are examined, including the roles of temperature sensitive afferent neurons as well as NO and other mediators. Factors that can modulate control mechanisms of the cutaneous vasculature, such as gender, aging, and clinical conditions, are discussed, as are nonthermoregulatory reflex modifiers of thermoregulatory cutaneous vascular responses.

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No direct role for A1/A2 adenosine receptor activation to reflex cutaneous vasodilatation during whole‐body heat stress in humans

Abstract: These data suggest A1/A2 adenosine receptor activation does not directly contribute to cutaneous active vasodilatation; however, a role for A1/A2 adenosine receptor activation is unmasked when NO synthase is inhibited.

Cited by 18 publications

References 36 publications

Adenosine receptor inhibition attenuates the decrease in cutaneous vascular conductance during whole‐body cooling from hyperthermia

Adenosine receptor inhibition attenuates the decrease in cutaneous vascular conductance during whole‐body cooling from hyperthermia

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

Cutaneous Vasodilator and Vasoconstrictor Mechanisms in Temperature Regulation

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