Thromboxane A2 in the paraventricular hypothalamic nucleus mediates glucoprivation-induced adrenomedullary outflow.

摘要: Glucoprivation stimulates a rapid sympathetic response to release and/or secrete catecholamines into the bloodstream. However, central regulatory mechanisms involving adrenoceptors and prostanoids production in paraventricular hypothalamic nucleus (PVN) that are responsible for glucoprivation-induced elevation of plasma still unresolved. In this study, we aimed clarify whether activation noradrenergic neurons projecting PVN can induce α- β-adrenergic receptor elevate catecholamine levels. We examined effects antagonists, cyclooxygenase inhibitor, thromboxane A synthase PGE2 subtype EP3 antagonist on intravenously administered 2-deoxy-D-glucose (2-DG)-induced noradrenaline levels freely moving rats. addition, 2-DG increase microdialysates. Intracerebroventricular (i.c.v.) pretreatment with phentolamine (a non-selective α-adrenergic antagonist) suppressed 2-DG-induced level adrenaline, whereas i.c.v. propranolol noradrenaline. I.c.v. indomethacin inhibitor) furegrelate attenuated elevations both adrenaline Furthermore, administration elevated B2 level, metabolite A2 Our results suggest brain including then PVN, which essential