α1-Adrenoceptor activation is involved in the central N-methyl-d-aspartate-induced adrenomedullary outflow in rats

摘要: Abstract N -methyl- d -aspartate (NMDA) has been implicated in the regulation of several autonomic responses brain. The present study determined whether activation α 1 -adrenoceptors is involved centrally administered NMDA-induced adrenomedullary catecholamine outflow, using urethane-anesthetized rats. NMDA (5.0 nmol/animal, i.c.v.)-induced elevation plasma levels noradrenaline and adrenaline was reduced by phentolamine (0.33 µmol/animal, i.c.v.), a non-selective α-adrenoceptor antagonist, 2-{[b-(4-hydroxyphenyl)ethyl]aminomethyl}-1tetralone (HEAT) (90.0 nmol/animal, selective -adrenoceptor antagonist. In contrast, sotalol (0.8 µmol/animal, β - adrenoceptor did not alter responses. addition, U-73122, phospholipase C inhibitor RHC-80267, diacylglycerol lipase (1.3 μmol/animal, i.c.v.) URB 602, monoacylglycerol (0.85 1.7 µmol/animal, both catecholamines. Furthermore, perfusion hypothalamic paraventricular nucleus with (0.3 1.0 mM) dose-dependently elevated levels. These were abolished co-administration dizocilpine malate (MK-801, 0.1 mM), non-competitive antagonist receptor (+)-S-145 (2.5 mM), competitive thromboxane A 2 receptor. results suggest that central outflow signaling cascades downstream may play an important role process.