Mechanisms of vasoactive intestinal peptide-mediated vasodilation in human skin

Wilkins, Brad W.; Chung, Linda H.; Tublitz, Nathan J.; Wong, Brett J.

doi:10.1152/japplphysiol.00366.2004

Cited by 62 publications

(65 citation statements)

References 47 publications

(62 reference statements)

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“…It has been demonstrated that NO contributes significantly to active vasodilation (21,33), and the vasodilation induced by a number of possible substances involved in active vasodilation (36,39,41,42). Along these lines, NO has also been observed to increase the biosynthesis of prostanoids in numerous experimental models.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, there appears to be some overlap in the vasodilatory pathways of these substances in the skin, particularly, with respect to NO. In human skin, VIP has been shown to have both NO and H 1 -receptor components (39); ACh has been shown to be partially dependent on NO in some (23,36), but not all, studies (17); and H 1 -receptor activation also appears to have a NOdependent component (42).…”

mentioning

confidence: 99%

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Prostanoids contribute to cutaneous active vasodilation in humans

McCord

Cracowski²,

Minson³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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140

158

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The specific mechanisms by which skin blood flow increases in response to a rise in core body temperature via cutaneous active vasodilation are poorly understood. The primary purpose of this study was to determine whether the cyclooxygenase (COX) pathway contributes to active vasodilation during whole body heat stress (protocol 1; n = 9). A secondary goal was to verify that the COX pathway does not contribute to the cutaneous hyperemic response during local heating (protocol 2; n = 4). For both protocols, four microdialysis fibers were placed in forearm skin. Sites were randomly assigned and perfused with 1) Ringer solution (control site); 2) ketorolac (KETO), a COX-1/COX-2 pathway inhibitor; 3) NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor; and 4) a combination of KETO and L-NAME. During the first protocol, active vasodilation was induced using whole body heating with water-perfused suits. The second protocol used local heaters to induce a local hyperemic response. Red blood cell flux (RBC flux) was indexed at all sites using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC; RBC flux/mean arterial pressure) was normalized to maximal vasodilation at each site. During whole body heating, CVC values at sites perfused with KETO (43 +/- 9% CVCmax), L-NAME (35 +/- 9% CVCmax), and combined KETO/L-NAME (22 +/- 8% CVCmax) were significantly decreased with respect to the control site (59 +/- 7% CVCmax) (P < 0.05). Additionally, CVC at the combined KETO/L-NAME site was significantly decreased compared with sites infused with KETO or L-NAME alone (P < 0.05). In the second protocol, the hyperemic response to local heating did not differ between the control site and KETO site or between the L-NAME and KETO/L-NAME site. These data suggest that prostanoids contribute to active vasodilation, but do not play a role during local thermal hyperemia.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Prostanoids contribute to cutaneous active vasodilation in humans

McCord

Cracowski²,

Minson³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

140

158

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“…Another likely explanation for our findings is that there are different mechanisms mediating the early and late phase of reflex vasodilation and that our interventions were selective for the later phase. Although NO is involved in both the early and the late phase of active vasodilation, the upstream pathways mediating NO release may be different, with acetylcholine and VIP contributing to the early phase and H 1 receptor activation contributing to the later phase through NO-dependent mechanisms (26,33,37,38).…”

Section: Discussionmentioning

confidence: 99%

“…Cutaneous active vasodilation is purportedly mediated by the cotransmission of acetylcholine and an unknown neurotransmitter(s) from the sympathetic vasodilator system (16). Furthermore, nitric oxide (NO) is required for full expression of cutaneous active vasodilation and contributes ϳ30% of the total vasodilatory response, where histamine and vasoactive intestinal peptide contribute to active vasodilation through NO-dependent mechanisms (4,15,26,32,37,38).Human aging in the absence of overt pathology is associated with attenuated reflex cutaneous vasodilation (17, 18). Aged humans have a reduced functional cotransmitter(s) contribution to the increase in skin blood flow during hyperthermia and rely predominantly on NO-dependent mechanisms (13), despite the fact that cutaneous NO-dependent vasodilation is compromised with advancing age (28).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

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Acute ascorbate supplementation alone or combined with arginase inhibition augments reflex cutaneous vasodilation in aged human skin

Holowatz¹,

Thompson²,

Kenney³

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Full expression of reflex cutaneous vasodilation (VD) is dependent on nitric oxide (NO) and is attenuated in older humans. NO may be decreased by an age-related increase in reactive oxygen species or a decrease in L-arginine availability via upregulated arginase. The purpose of this study was to determine the effect of acute antioxidant supplementation alone and combined with arginase inhibition on reflex VD in aged skin. Eleven young (Y; 22 +/- 1 yr) and 10 older (O; 68 +/- 1 yr) human subjects were instrumented with four intradermal microdialysis (MD) fibers. MD sites were control (Co), NO synthase inhibited (NOS-I), L-ascorbate supplemented (Asc), and Asc + arginase-inhibited (Asc + A-I). After baseline measurements, subjects underwent whole body heating to increase oral temperature (T(or)) by 0.8 degrees C. Red blood cell flux was measured by using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated (CVC = flux/mean arterial pressure) and normalized to maximal (CVC(max)). VD during heating was attenuated in O (Y: 37 +/- 3 vs. O: 28 +/- 3% CVC(max); P< 0.05). NOS-I decreased VD in both groups compared with Co (Y: 20 +/- 4; O: 15 +/- 2% CVC(max); P < 0.05 vs. Co within group). Asc and Asc + A-I increased VD beyond Co in O (Asc: 35 +/- 4% CVC(max); Asc + A-I: 41 +/- 3% CVC(max); P < 0.001) but not in Y (Asc: 36 +/- 3% CVC(max); Asc + A-I: 40 +/- 5% CVC(max); P > 0.05). Combined Asc + A-I resulted in a greater increase in VD than Asc alone in O (P = 0.001). Acute Asc supplementation increased reflex VD in aged skin. Asc combined with arginase inhibition resulted in a further increase in VD above Asc alone, effectively restoring CVC to the level of young subjects.

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Cutaneous Vasodilator and Vasoconstrictor Mechanisms in Temperature Regulation

Johnson

Minson

Kellogg

2014

Comprehensive Physiology

322

286

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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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Mechanisms of vasoactive intestinal peptide-mediated vasodilation in human skin

Cited by 62 publications

References 47 publications

Prostanoids contribute to cutaneous active vasodilation in humans

Prostanoids contribute to cutaneous active vasodilation in humans

Acute ascorbate supplementation alone or combined with arginase inhibition augments reflex cutaneous vasodilation in aged human skin

Cutaneous Vasodilator and Vasoconstrictor Mechanisms in Temperature Regulation

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