CENTRAL NOREPINEPHRINE RELEASE AND ENVIRONMENTAL STRESS

该应用是基于微透析实验，其中NE释放 同时从室旁（PVN）和后壁监测 自由活动大鼠下丘脑核（PH）的前， 在施加了一个可量化的、无痛的环境压力后， “震动压力”。 震动器的压力会引起立即的升压效应，心脏 速率改变，并增加下丘脑两个部位NE的释放; 应激后平均动脉压（MAP）和心率（HR）恢复至 对照水平，但增强的NE释放持续，在PH比PVN更长。 具体的目标是集中在测试假设，心血管 这些变化部分或全部不依赖于下丘脑NE的释放 在振动器压力和升压反应减弱 下丘脑NE释放。 自发性高血压大鼠（SHR）有一个 对震动压力的过度升压反应 我们假设SHR 下丘脑NE释放的模式大于和/或不同于 控制，肾上腺素受体调节的释放是不同的SHR 比对照组。 最后探讨了应激后NE释放增强的机制 PVN和PH将被确定。 协议要求持续测量 MAP和HR，同时采集5分钟透析液 样品，用PVN和PH中的1 mm长微透析探针获得，来自 自由移动的老鼠 细胞外NE将通过敏感的 放射酶测定 这些研究将提供关于中央 去甲肾上腺素能和心血管活动的整合机制 高血压和压力。

This application is based on microdialysis experiments in which NE release was monitored simultaneously from paraventricular (PVN) and posterior nucleus (PH) of the hypothalamus in the freely moving rats before, during and after imposition of a quantifiable, painless, environmental stressor, "shaker stress". Shaker stress cause an immediate pressor effect, heart rate change and increases the release of NE at both hypothalamic sites; after stress mean arterial pressure (MAP) and heart rate (HR) return to control levels but enhanced NE release persists, longer in PH than PVN. Specific aims are focused to test the hypotheses that cardiovascular changes are, in part or totally, independent of hypothalamic NE release during shaker stress and that the pressor response attenuates the hypothalamic NE release. Spontaneously hypertensive rats (SHR) have an exaggerated pressor response to shaker stress. We hypothesize that SHR have a greater and/or different pattern of hypothalamic NE release than controls and that adrenoceptor modulation of release is different in SHR than controls. Finally the mechanism of post-stress, enhanced NE release in PVN and PH will be determined. Protocols require continuous measurement of MAP and HR and the simultaneous collection of 5 minute dialysate samples, obtained with 1 mm long microdialysis probes in PVN and PH, from freely moving rats. Extracellular NE will be measured by sensitive radioenzymatic assay. These studies will provide new data on central integrative mechanisms of noradrenergic and cardiovascular activity in hypertension and during stress.