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      Current-Induced Vasodilation during Water Iontophoresis (5 min, 0.10 mA) Is Delayed from Current Onset and Involves Aspirin Sensitive Mechanisms

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          Study of the microcirculation by iontophoresis is potentially confounded by any non-specific effects of current application. Laser Doppler flow (LDF, mean ± SD; arbitrary units; AU) was recorded on the forearms of healthy volunteers during and 20 min following application of 0.10-mA current for 1, 3 and 5 min, using deionised water as a vehicle. Local heating to 44°C was then applied for 24 min to assess maximal vasodilation. Cathodal current applications resulted in delayed and prolonged vasodilation (peak values: 78 ± 29, 75 ± 19, 80 ± 37 AU) whereas anodal peak LDF was 13 ± 6, 27 ± 34 and 72 ± 40 AU for 1-, 3- and 5-min periods of current applications, respectively. From current onset, inflexion points in the responses to 3- and 5-min anodal current applications occurred at 4.5 and 6.5 min, respectively, and at ∼1.5 min for all cathodal current applications. For 5-min current applications: a preliminary tourniquet ischaemia neither changed the time course nor the amplitude of the response to current application. In this situation, local anaesthesia abolished the current-induced vasodilation. Chronic capsaicin pretreatment decreased the amplitude of the vasodilation. Pretreatment with 500 mg oral aspirin decreased the cathodal vasodilation and abolished the anodal vasodilation, even in the absence of preliminary ischaemia. We conclude that vasodilation to prolonged application of 0.10-mA continuous monopolar current after transient tourniquet ischaemia cannot be exclusively the result of an axon reflex initiated by current onset. This current-induced vasodilation is at least partly dependent on capsaicin-sensitive afferent fibres and relies on aspirin-sensitive mechanisms at both polarities.

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          Most cited references 12

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          The anti-inflammatory agents aspirin and salicylate inhibit the activity of I(kappa)B kinase-beta.

          NF-kappaB comprises a family of cellular transcription factors that are involved in the inducible expression of a variety of cellular genes that regulate the inflammatory response. NF-kappaB is sequestered in the cytoplasm by inhibitory proteins, I(kappa)B, which are phosphorylated by a cellular kinase complex known as IKK. IKK is made up of two kinases, IKK-alpha and IKK-beta, which phosphorylate I(kappa)B, leading to its degradation and translocation of NF-kappaB to the nucleus. IKK kinase activity is stimulated when cells are exposed to the cytokine TNF-alpha or by overexpression of the cellular kinases MEKK1 and NIK. Here we demonstrate that the anti-inflammatory agents aspirin and sodium salicylate specifically inhibit IKK-beta activity in vitro and in vivo. The mechanism of aspirin and sodium salicylate inhibition is due to binding of these agents to IKK-beta to reduce ATP binding. Our results indicate that the anti-inflammatory properties of aspirin and salicylate are mediated in part by their specific inhibition of IKK-beta, thereby preventing activation by NF-kappaB of genes involved in the pathogenesis of the inflammatory response.
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            Flare and Itch Induced by Substance P in Human Skin

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              Peripheral pain mechanisms.

              Our understanding of the cellular and molecular bases of transduction of painful stimuli has burgeoned in the past year, mainly as a result of studies on isolated sensory neurones in culture. The ion channels underlying neuronal responses to noxious heat, to protons and to ATP have recently been characterized. The typical increase in nociceptor sensitivity produced by tissue damage has been found to be mediated by at least two distinct mechanisms. In the first, bradykinin augments the current activated by heat through a mechanism that involves activation of protein kinase C. In a second sensitization mechanism, prostaglandin E2 alters the voltage threshold of several ion channels, including a novel tetrodotoxin-insensitive Na+ channel, in such a way that initiation of action potentials is facilitated.

                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                February 2002
                13 February 2002
                : 39
                : 1
                : 59-71
                Laboratory of Physiology, University Hospital, Angers, France
                48994 J Vasc Res 2002;39:59–71
                © 2002 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 2, References: 71, Pages: 13
                Research Paper


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