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.

journal_name

Eur J Pharmacol

authors

Okada S,Yamaguchi-Shima N,Shimizu T,Arai J,Yorimitsu M,Yokotani K

doi

10.1016/j.ejphar.2008.02.069

subject

Has Abstract

pub_date

2008-05-31 00:00:00

pages

145-50

issue

1-3

eissn

0014-2999

issn

1879-0712

pii

S0014-2999(08)00263-X

journal_volume

586

pub_type

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