title: Centrally administered N-methyl-d-aspartate evokes the adrenal secretion of noradrenaline and adrenaline by brain thromboxane A2-mediated mechanisms in rats.
abstract: 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 micromol/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 micromol/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.
authors: Department of Pharmacology: Graduate School of Medicine, Kochi University, Nankoku, Kochi 783-8505, Japan. okadas@kochi-u.ac.jp
authors: Shoshiro
authors: S
authors: Okada
authors: Naoko
authors: N
authors: Yamaguchi-Shima
authors: Takahiro
authors: T
authors: Shimizu
authors: Junichi
authors: J
authors: Arai
authors: Mieko
authors: M
authors: Yorimitsu
authors: Kunihiko
authors: K
authors: Yokotani
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000315:Adrenalectomy; D000771:Anesthesia, Intravenous; D018686:Anesthetics, Intravenous; D000818:Animals; D001923:Brain Chemistry / Q000502:physiology*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004837:Epinephrine / Q000378:metabolism*; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D007276:Injections, Intraventricular; D008297:Male; D016202:N-Methylaspartate / Q000037:antagonists & inhibitors / Q000097:blood / Q000494:pharmacology*; D009638:Norepinephrine / Q000378:metabolism*; D011453:Prostaglandins / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D013268:Stimulation, Chemical; D013928:Thromboxane A2 / Q000502:physiology*; D013930:Thromboxane-A Synthase / Q000037:antagonists & inhibitors; D014520:Urethane
chemical_list: D018686:Anesthetics, Intravenous; D016861:Cyclooxygenase Inhibitors; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D011453:Prostaglandins; D016194:Receptors, N-Methyl-D-Aspartate; D014520:Urethane; D013928:Thromboxane A2; D016202:N-Methylaspartate; D013930:Thromboxane-A Synthase; D009638:Norepinephrine; D004837:Epinephrine