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背内侧下丘脑核和穹窿周区对压力感受器反射的调节作用。

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

作者信息

McDowall Lachlan M, Horiuchi Jouji, Killinger Suzanne, Dampney Roger A L

机构信息

Department of Physiology, University of Sydney, NSW 2006, Australia.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2006 Apr;290(4):R1020-6. doi: 10.1152/ajpregu.00541.2005. Epub 2005 Nov 10.

Abstract

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.

摘要

位于经典下丘脑防御区内的下丘脑背内侧核(DMH)和穹窿周区(PeF)中的神经元,负责对心理应激产生心血管反应。先前的研究表明,电刺激下丘脑防御区会抑制压力感受器反射的心脏和(某些情况下的)交感神经成分。相比之下,自然诱发的心理应激似乎与这种抑制无关。在本研究中,我们测试了特异性激活DMH和PeF内的神经元对乌拉坦麻醉大鼠肾交感神经活动和心率的压力反射控制的影响。向DMH微量注射荷包牡丹碱(一种GABA(A)受体拮抗剂)会导致心率和肾交感神经活动呈剂量依赖性增加,将这两个变量的压力反射控制转移到更高水平(即增加压力反射功能曲线 的上下平台,并增加平均动脉压的阈值、中点和饱和水平)。压力反射交感神经成分的最大增益也增加了,而心脏成分的最大增益没有显著变化。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。向PeF微量注射荷包牡丹碱会诱发非常相似的效果。结果表明,DMH/PeF区域神经元的去抑制不仅会增加交感血管运动活动和心率,还会重置压力感受器反射,使其在更高的动脉压工作范围内保持有效,且敏感性不会降低。

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