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Inhibition of a peripheral sympathetic-cholinergic system by presynaptic α2-adrenoceptors

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Summary

Intravenous administration of catecholamines produced dose-related inhibition of electrodermal responses (EDRs) evoked by electrical stimulation of the post-ganglionic sciatic nerve in anaesthetized rats, with relative potencies being (−)-adrenaline > (±)-adrenaline > (−)-noradrenaline = (+)-adrenaline. The suppression of EDRs by (±)-adrenaline and (−)-noradrenaline was blocked by pretreatment with yohimbine (0.75 mg/kg i.v.) but not by prazosin (0.3 mg/kg i. v.). The selective α2-adrenoceptor agonist B-HT 920 also inhibited neurally evoked skin potential responses. This effect of B-HT 920 was antagonized by the selective α2-adrenoceptor antagonist idazoxan (0.1 mg/kg i. v.) but was insensitive to prazosin. Idazoxan was more potent than yohimbine in blocking (±)-adrenaline-induced suppression of EDRs. Methacholine administered into the femoral artery evoked EDRs by an atropine-sensitive mechanism. Methacholine-induced EDRs were not suppressed by intravenous administration of (−)-adrenaline (1 μg/kg or 3 μg/ kg) whereas EDRs evoked by the sciatic nerve stimulation on the other hindpaw were inhibited. Increase in the endogenous catecholamines by asphyxia strongly inhibited EDRs by a mechanism which was also sensitive to yohimbine but not to prazosin. These results suggest that peripheral presynaptic α2-adrenergic mechanisms are involved in inhibition of transmitter release in this sympatheticcholinergic system.

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Ito, T., Koss, M.C. Inhibition of a peripheral sympathetic-cholinergic system by presynaptic α2-adrenoceptors. Naunyn-Schmiedeberg's Arch Pharmacol 337, 24–28 (1988). https://doi.org/10.1007/BF00169472

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  • DOI: https://doi.org/10.1007/BF00169472

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