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• W2072246563 abstract "We have previously shown that norepinephrine can produce hyperalgesia via an α2-adrenergic receptor mechanism. The α2-adrenergic receptor agonist clonidine has, however, also been shown to produce peripheral analgesia. In view of the multiple α2-subtypes currently known (i.e. α2A, α2Bandα2C), we evaluated the α2-receptor subtypes mediating norepinephrine-induced peripheral hyperalgesia and clonidine analgesia. Norepinephrine and the α2-adrenergic agonists clonidine and UK 14,304 (1–1000 ng), when co-injected with the calcium ionophore A23187 (1000 ng) produced dose-dependent hyperalgesia in the Randall-Selitto paw withdrawal test. Norepinephrine (100 ng) hyperalgesia was dose-dependently antagonized by α2-adrenergic receptor antagonists. From the estimated ID50, the rank order of potency was: SK&F 104856 (α2B) ≅ imiloxan (α2B) rauwolscine (α2C) ≫ BRL 44408 (α2A). Norepinephrine hyperalgesia was not significantly affected by pertussis-toxin treatment. Prostaglandin E2 (100 ng) hyperalgesia was inhibited dose-dependently, by clonidine and UK 14,304. Rauwolscine was more potent in reversing the inhibitory effect of clonidine on prostaglandin E2 than imiloxan while BRL 44408 was ineffective. The inhibitory effect of clonidine on prostaglandin E2 hyperalgesia was reversed by pertussis toxin. These data suggest that α2B-subtype receptors mediate (norepinephrine hyperalgesia while the antinociceptive effect of α2-agonist is mediated by the α2C-subtype receptor. Differential coupling of these receptor subtypes to second messenger systems and location on different cell types in the rat paw may explain, at least in part, their differential responses to α2-agonist stimulation, leading to hyperalgesia and analgesia." @default.
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• W2072246563 date "1995-05-01" @default.
• W2072246563 modified "2023-10-10" @default.
• W2072246563 title "Peripheral nociceptive effects of α2-adrenergic receptor agonists in the rat" @default.
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• W2072246563 doi "https://doi.org/10.1016/0306-4522(94)00562-j" @default.
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