Epinephrine exacerbates arthritis by an action at presynaptic B2-adrenoceptors
Sympathetic efferents contribute to the severity of joint injury in experimental arthritis in the rat, [Levine J.D. et al. (1986) J. Neurosci. 6, 3423-3429] and beta2-adrenergic receptor antagonists suppress the disease [Levine J.D. et al. (1988) Proc. natn. Acad. Sci. U.S.A. 85, 4553-4556]. The present study was directed at determining the endogenous ligand for, and target of, the beta2-receptor contribution to arthritis. We report that adrenal medullectomy significantly reduced joint injury in experimental arthritis, but that severe joint injury was re-established in adrenal medullectomized rats chronically treated with epinephrine or the beta2-agonist, salbutamol. The ability of these two drugs to enhance joint injury in adrenal medullectomized rats was blocked by sympathectomy. These data suggest that adrenal medulla-derived epinephrine acts at beta2-adrenoceptors on sympathetic efferent nerve terminals, to contribute to the severity of experimental arthritis.
Coderre, TJ; Basbaum, AI; Dallman, MF; Helms, C; Levine, JD
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