Sympathetic-dependence in bradykinin-induced synovial plasma extravasation is dose-related
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Cited by (38)
5.21 - Sympathetic Nervous System and Pain
2020, The Senses: A Comprehensive Reference: Volume 1-7, Second EditionEffects on hemodynamic variables and echocardiographic parameters after a stellate ganglion block in 15 healthy volunteers
2016, Autonomic Neuroscience: Basic and ClinicalFunction of the sympathetic supply in acute and chronic experimental joint inflammation
2014, Autonomic Neuroscience: Basic and ClinicalCitation Excerpt :Sympathectomy reduced plasma extravasation evoked by infusion of bradykinin into the knee joint of the rat whereas pretreatment with capsaicin did not attenuate this reaction (Coderre etal., 1989). Bradykinin-evoked plasma extravasation into the knee joint (from postcapillary venules) was also reduced 7 and 14 days after surgical sympathectomy (Miao etal., 1996a,b). Interestingly, this effect was not observed after section of the preganglionic fibers projecting to the lumbar sympathetic ganglia suggesting that this particular sympathetic function does neither depend on the input from the central sympathetic system nor on action potentials in these fibers (Miao et al., 1996b).
Acute inflammation in the joint: Its control by the sympathetic nervous system and by neuroendocrine systems
2014, Autonomic Neuroscience: Basic and ClinicalCitation Excerpt :As expected, activation of the sympathetic postganglionic neurons by electrical stimulation of the lumbar sympathetic chain at frequencies of 0.2 to 5 Hz reduces both resting and BK-induced PE as well as plasma extravasation during infusion of platelet activating factor because the blood flow through the synovium is reduced (Miao et al., 1996a). Quantitative analysis of the synovial plasma extravasation generated by different concentrations of bradykinin in the perfusate shows that the sympathetically mediated component is particularly large at bradykinin concentrations which have been measured in inflamed tissues (between 10− 8 and 3 × 10− 7 M [black bar in Fig. 3]; Hargreaves et al., 1993; Swift et al., 1993) and almost undetectable at higher (pharmacological) concentrations (≥ 10− 6 M) as shown by Cambridge and Brain (1995), probably because bradykinin also acts directly on the endothelial cells at these high concentrations and because this direct endothelial effect is maximal at pharmacological bradykinin concentrations (Fig. 3) (Miao et al., 1996b). These types of experiments suggest that sympathetic postganglionic neurons innervating the joint capsule and its synovium have two functions (Fig. 4): first, to regulate blood flow (vasoconstrictor function), and second, to mediate vascular permeability.
Neurogenic Regulation of Bradykinin-Induced Synovitis
2009, NeuroImmune BiologyCitation Excerpt :Furthermore, the sympathetic nervous system may play a regulatory role in secondary lymphoid organs as it has been shown that selective sympathectomy in secondary lymphoid organs exacerbates experimental arthritis [16,101]. Perfusion of bradykinin through the synovium produces a marked increase in the magnitude of plasma extravasation [73,84,90,91,97,102–104]. In patients with joint pain, there is a positive correlation between concentration of bradykinin in the synovium and magnitude of synovitis [105], with an increase in expression of the constitutive G-protein-coupled bradykinin B2 receptors [106].
Complex Regional Pain Syndromes
2008, The Senses: A Comprehensive Reference