Centrally applied nitric oxide donor elevates plasma corticosterone by activation of the hypothalamic noradrenergic neurons in rats

摘要: Abstract The present study was undertaken to investigate the mechanisms involved in a nitric oxide donor [3-morpholino-sydnonimine (SIN-1)]-induced activation of hypothalamic–pituitary–adrenal axis urethane- and α-chloralose-anesthetized rats. Intracerebroventricularly (i.c.v.) administered SIN-1 (250 500 μg/animal) effectively dose-dependently elevated plasma levels corticosterone. Pretreatment with phentolamine μg/animal, i.c.v.), an α-adrenoceptor antagonist, attenuated elevation corticosterone evoked by SIN-1, but sotalol (300 β-adrenoceptor without effects. same doses also increased release noradrenaline hypothalamic paraventricular nucleus (PVN) measuring microdialysis technique, this increase abolished tetrodotoxin (1 μM) into perfusion solution PVN. Furthermore, pretreatment indomethacin (500 cyclooxygenase inhibitor, SIN-1-induced elevations both PVN These results suggest that i.c.v. activates central noradrenergic neurons innervating prostaglandin-mediated mechanisms. Released elevates via α-adrenoreceptors