Regular ArticleReceptor-Mediated Stimulation and Inhibition of Nerve Growth Factor Secretion by Vascular Smooth Muscle
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Inflammation in CRPS: Role of the sympathetic supply
2014, Autonomic Neuroscience: Basic and ClinicalCitation Excerpt :This effect was reversed after catecholamine depletion or an IL-6-antagonist (Li et al., 2013). Postganglionic sympathetic neurons might modulate inflammatory reactions, either directly by releasing prostaglandins (Gonzales et al., 1991) or indirectly by releasing NGF from vascular smooth muscle cells (Tuttle et al., 1993) or the bladder (Schnegelsberg et al., 2010). As noted above, the sympathetic nervous system influences innate immunity via dendritic cells, which are modulated by adrenoreceptors: α1-adrenoceptors stimulate and β2-adrenoceptors inhibit dendritic cell migration and immune system activation (Maestroni, 2006).
Inflammation contributes to axon reflex vasodilatation evoked by iontophoresis of an alpha-1 adrenoceptor agonist
2011, Autonomic Neuroscience: Basic and ClinicalCitation Excerpt :Nevertheless, iontophoresis of noradrenaline evoked an axon reflex in the human forearm that was blocked by pretreatment with a local anaesthetic cream (Drummond and Lipnicki, 1999), and iontophoresis of the α1-adrenoceptor agonist methoxamine evoked vasodilatation in nearby skin that was blocked by pretreatment with the α1-adrenoceptor antagonist terazosin (Drummond, 2009b). Together, these findings suggest that α1-adrenoceptors modulate the sensitivity of peripheral C-fibre nociceptors, either directly (Nicholson et al., 2005) or by releasing inflammatory agents such as nerve growth factor or prostaglandin E2 from secondary target cells (Tuttle et al., 1993; Trevisani et al., 2007; Kopp et al., 2007). Adrenergic vasoconstriction (Drummond, 2002; Thompson et al., 2005) might intensify these effects by reducing the dispersal of inflammatory mediators.
Nerve Growth Factor in Rheumatic Diseases
2010, Seminars in Arthritis and RheumatismCitation Excerpt :The release of these neuropeptides may lead to neurogenic inflammation, thereby enhancing vascular headache (185-188). Vascular smooth muscle cells express NGF (189) and, following its release, the activation of TrkA subsequently modulates nociceptors (190,191). Saldanha and coworkers examined the superficial temporal artery of 17 patients with headache (192).
Alpha-1 adrenoceptor stimulation triggers axon-reflex vasodilatation in human skin
2009, Autonomic Neuroscience: Basic and ClinicalDepletion of noradrenaline inhibits electrically-evoked pain in the skin of the human forearm
2008, European Journal of Pain