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Noradrenaline‐Induced Prostaglandin Production by Sympathetic Postganglionic Neurons Is Mediated by α2‐Adrenergic Receptors
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AbstractIn this study we have demonstrated that noradrenaline increases the levels of prostaglandin E2 and prostaglandin I2 (detected as the stable metabolite 6‐keto‐prostaglandin F1α) synthesized by homogenates of superior cervical ganglia from the adult rat. This noradrenaline‐induced prostaglandin production was further characterized: (a) Selective destruction of adrenergic sympathetic postganglionic neurons in the ganglia using 6‐hydroxydopamine abolished both basal and stimulated prostaglandin production, (b) Elimination of preganglionic cholinergic sympathetic nerve terminals in the ganglia had no effect, (c) Mepacrine (a phospholipase inhibitor) and indomethacin (a cyclooxygenase inhibitor) attenuated both basal and stimulated prostaglandin production. (d) Yohimbine, but not prazosin, suppressed the noradrenaline dose‐response curve for prostaglandin production. The results of these experiments show that, in vitro, noradrenaline stimulates de novo synthesis of prostaglandin E2 and prostaglandin I2 by sympathetic postganglionic neurons. This stimulation by noradrenaline appears to result from action at an α2‐adrenergic receptor.
Title: Noradrenaline‐Induced Prostaglandin Production by Sympathetic Postganglionic Neurons Is Mediated by α2‐Adrenergic Receptors
Description:
AbstractIn this study we have demonstrated that noradrenaline increases the levels of prostaglandin E2 and prostaglandin I2 (detected as the stable metabolite 6‐keto‐prostaglandin F1α) synthesized by homogenates of superior cervical ganglia from the adult rat.
This noradrenaline‐induced prostaglandin production was further characterized: (a) Selective destruction of adrenergic sympathetic postganglionic neurons in the ganglia using 6‐hydroxydopamine abolished both basal and stimulated prostaglandin production, (b) Elimination of preganglionic cholinergic sympathetic nerve terminals in the ganglia had no effect, (c) Mepacrine (a phospholipase inhibitor) and indomethacin (a cyclooxygenase inhibitor) attenuated both basal and stimulated prostaglandin production.
(d) Yohimbine, but not prazosin, suppressed the noradrenaline dose‐response curve for prostaglandin production.
The results of these experiments show that, in vitro, noradrenaline stimulates de novo synthesis of prostaglandin E2 and prostaglandin I2 by sympathetic postganglionic neurons.
This stimulation by noradrenaline appears to result from action at an α2‐adrenergic receptor.
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