Rodriguez-Martinez M, Jones S Y, DiBona G F
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242, USA.
J Hypertens. 1995 Dec;13(12 Pt 1):1449-55.
This investigation examined the central portion of the cardiac volume receptor reflex, which mediates the exaggerated renal sympathoinhibitory response to isotonic saline volume loading observed in spontaneously hypertensive rats, and compared the findings with those in normotensive Wistar-Kyoto control rats.
Wistar-Kyoto and spontaneously hypertensive rats were fed either a normal diet or one high in sodium chloride for 4 weeks and subjected to sinoaortic denervation. To evaluate the central gain of the cardiopulmonary baroreflex, electrical stimulation of the central portion of the cut vagus was used to provide a standardized stimulus that simulates activation of cardiac volume receptors. To evaluate central alpha 2-adrenoceptor regulation of renal sympathetic nerve activity, volume loading was performed in rats pretreated with intracerebroventricular guanabenz, which decreased the elevated basal values of arterial pressure, heart rate and renal sympathetic nerve activity in spontaneously hypertensive rats towards those of Wistar-Kyoto rats.
Vagal stimulation produced frequency-dependent decreases in arterial pressure, heart rate and renal sympathetic nerve activity that were similar in the two strains of rats on either a normal- or a high-sodium diet. Volume administration in rats pretreated with guanabenz resulted in similar decreases in renal sympathetic nerve activity in the two strains of rats.
The mechanism of exaggerated renal sympathoinhibition during volume administration in spontaneously hypertensive rats involves an alteration in central alpha 2-adrenoceptor regulation of renal sympathetic nerve activity.
本研究检测了心脏容量感受器反射的中枢部分，该部分介导了自发性高血压大鼠对等渗盐水容量负荷的过度肾交感神经抑制反应，并将结果与正常血压的Wistar-Kyoto对照大鼠进行比较。
将Wistar-Kyoto大鼠和自发性高血压大鼠分别给予正常饮食或高氯化钠饮食4周，然后进行窦主动脉去神经支配。为评估心肺压力反射的中枢增益，采用电刺激切断迷走神经的中枢部分，以提供模拟心脏容量感受器激活的标准化刺激。为评估肾交感神经活动的中枢α2-肾上腺素能受体调节，对脑室注射胍那苄预处理的大鼠进行容量负荷，胍那苄可使自发性高血压大鼠升高的动脉压、心率和肾交感神经活动的基础值降至Wistar-Kyoto大鼠水平。
迷走神经刺激使动脉压、心率和肾交感神经活动呈频率依赖性降低，在正常或高钠饮食的两种大鼠品系中相似。胍那苄预处理的大鼠进行容量给药后，两种大鼠品系的肾交感神经活动均有相似程度的降低。
自发性高血压大鼠容量给药期间肾交感神经抑制过度的机制涉及肾交感神经活动中枢α2-肾上腺素能受体调节的改变。
