糖皮质激素在孤束核内对去甲肾上腺素/神经肽Y引起的心血管效应的影响及其机制

Effects of Glucocorticoids on Cardiovascular Response after Microinjection of NoradrenalineNeuropeptide Y into Nucleus Tractus Solitarius and the Underlying Mechanism in Rats

本研究观察了糖皮质激素自身在孤束核（ＮＴＳ）内的心血管效应，以及它在ＮＴＳ内对ＮＡＮＰＹ诱导的心血管活动变化的影响及机制。结果发现，大剂量地塞米松（Ｄｅｘ）在大鼠ＮＴＳ内能很快导致血压下降，血清中ＮＯ浓度升高。小剂量Ｄｅｘ在ＮＴＳ内能很快抑制ＮＡＮＰＹ在ＮＴＳ内诱导的心血管效应，并维持较长时间。表明Ｄｅｘ对ＮＡＮＰＹ在ＮＴＳ诱导的心血管效应的抑制作用可能有基因和非基因两种途径参与。进一步分析它的非基因机制发现这种快速抑制作用与胞内糖皮质激素受体无关，而是通过兴奋ＧＡＢＡＡ受体，降低减压反射；或者降低α２受体的敏感性，抑制ＮＯ的形成；或者直接作用于细胞膜上的离子通道以影响它们对ＮＡＮＰＹ的反应；

The present study was designed to observe the effect of glucocorticoids in the NTS on cardiovascular regulation, and to explore the effect of glucocorticoids on cardiovascular responses to microinjection of NANPY into the NTS. A large dosage of Dex was found to evoke a decrease of blood pressure and heart rate, and an increase of serum NO concentration. A small dosage of Dex rapidly attenuated or even abolished the cardiovascular responses to NANPY microinjected into NTS, and this effect continued for a longer period. It indicates that the effect of Dex on cardiovascular responses to NANPY is mediated through both the genomic and nongenomic pathways. As regards the nongenomic mechanism, it was found that the rapid inhibitory effect had nothing to do with the intracellular glucocorticoid receptors,but was mediated through the stimulation of GABAA receptor to decrease the depressor reflex, or decreasing the sensitivity of α2adrenergic receptor and inhibiting NO formation, or directly affecting the potassium and calcium channel in the membrane and altering the response of cardiovascular neurons in the NTS to NANPY.