...
首页> 外文期刊>American Journal of Physiology >Modulation of the baroreceptor reflex by the dorsomedial hypothalamic nucleus and perifornical area.
【24h】

Modulation of the baroreceptor reflex by the dorsomedial hypothalamic nucleus and perifornical area.

机译:丘脑下丘脑核和肾小管旁区域对压力感受器反射的调节。

获取原文
获取原文并翻译 | 示例

摘要

Neurons within the dorsomedial hypothalamic nucleus (DMH) and perifornical area (PeF), which lie within the classic hypothalamic defense area, subserve the cardiovascular response to psychological stress. Previous studies have shown that electrical stimulation of the hypothalamic defense area causes inhibition of the cardiac and (in some cases) sympathetic components of the baroreceptor reflex. In contrast, naturally evoked psychological stress does not appear to be associated with such inhibition. In this study, we tested the effect of specific activation of neurons within the DMH and PeF on the baroreflex control of renal sympathetic nerve activity and heart rate in urethane-anesthetized rats. Microinjection of bicuculline (a GABA(A) receptor antagonist) into the DMH caused dose-dependent increases in heart rate and renal sympathetic activity, shifted the baroreflex control of both variables to higher levels (i.e., increased the upper and lower plateaus of the baroreflex function curves, and increased the threshold, midpoint, and saturation levels of mean arterial pressure). The maximum gain of the sympathetic component of the baroreflex was also increased, while that of the cardiac component was not significantly changed. Increases in the midpoint were very similar in magnitude to the evoked increases in baseline mean arterial pressure. Microinjection of bicuculline into the PeF evoked very similar effects. The results indicate that disinhibition of neurons in the DMH/PeF region not only increases sympathetic vasomotor activity and heart rate but also resets the baroreceptor reflex such that it remains effective, without any decrease in sensitivity, over a higher operating range of arterial pressure.
机译:位于典型的下丘脑防御区域内的背丘脑下丘脑核(DMH)和肾小管旁区域(PeF)内的神经元可满足心血管对心理压力的反应。先前的研究表明,下丘脑防御区的电刺激会导致心脏压力感受器反射的心脏和(在某些情况下)交感神经成分受到抑制。相反,自然诱发的心理压力似乎与这种抑制作用无关。在这项研究中,我们测试了DMH和PeF中神经元的特异性激活对尿烷麻醉大鼠肾交感神经活动和心率的压力反射控制的影响。将双小分子(一种GABA(A)受体拮抗剂)微量注射到DMH中会引起心率和肾脏交感神经活性的剂量依赖性增加,将两个变量的压力反射控制都移至更高的水平(即,压力反射的上,下高原增加)功能曲线,并增加了平均动脉压的阈值,中点和饱和水平)。压力反射的交感成分的最大增益也增加了,而心脏成分的交感成分的最大增益没有明显改变。中点的增加幅度与诱发的基线平均动脉压增加幅度非常相似。将小分子双分子注射到PeF中引起了非常相似的效果。结果表明,DMH / PeF区神经元的抑制不仅增加了交感血管舒缩活性和心率,而且使压力感受器反射复位,从而在较高的动脉压操作范围内仍保持有效,而敏感性没有任何下降。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号