Centrally administered N-methyl-d-aspartate evokes the adrenal secretion of noradrenaline and adrenaline by brain thromboxane A₂-mediated mechanisms in rats

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• 作者：Shoshiro Okada ; Naoko Yamaguchi-Shima ; Takahiro Shimizu ; Junichi Arai ; Mieko Yorimitsu ; Kunihiko Yokotani
• 关键词：Adrenomedullary outflow ; Cyclooxygenase ; N-methyl-d-aspartate ; Plasma catecholamine ; Thromboxane A₂
• 刊名：European Journal of Pharmacology
• 出版年：2008
• 期刊代码：24_00142999
• 类别：neu
• 出版时间：31 May 2008
• 卷：586
• 期：1-3
• 页码：145-150
• 文件大小：549 K

摘要

Plasma adrenaline mainly originated from adrenaline-containing cells in the adrenal medulla, while plasma noradrenaline reflects the release from sympathetic nerves in addition to the secretion from noradrenaline-containing cells in the adrenal medulla. The present study was undertaken to characterize the source of plasma catecholamines induced by centrally administered N-methyl-d-aspartate with regard to the brain prostanoid, using urethane-anesthetized rats. Intracerebroventricularly (i.c.v.) administered N-methyl-d-aspartate (1.0, 5.0, 10.0 nmol/animal) dose-dependently elevated plasma levels of noradrenaline and adrenaline. The N-methyl-d-aspartate (5.0 nmol/animal, i.c.v.)-induced elevation of both catecholamines was reduced by dizocilpine maleate (5 nmol/animal, i.c.v.), a non-competitive N-methyl-d-aspartate receptor antagonist. Indomethacin (0.6 and 1.2 μmol/animal, i.c.v.), an inhibitor of cyclooxygenase, dose-dependently reduced the N-methyl-d-aspartate (5.0 nmol/animal, i.c.v.)-induced elevation of both catecholamines. The N-methyl-d-aspartate-induced response was dose-dependently attenuated by furegrelate (0.9 and 1.8 μmol/animal, i.c.v.), an inhibitor of thromboxane A₂ synthase. Furthermore, the acute bilateral adrenalectomy abolished the N-methyl-d-aspartate-induced responses, indicating that the source of increase in plasma noradrenaline evoked by N-methyl-d-aspartate is due to secretion from the adrenal gland and not due to release from sympathetic nerve terminals. These results suggest that centrally administered N-methyl-d-aspartate induces the secretion of noradrenaline and adrenaline from adrenal medulla by the brain thromboxane A₂-mediated mechanisms in rats.