SYMPATHETIC HYPERACTIVITY ELEVATES BLOOD-PRESSURE DURING ACUTE CEREBROVENTRICULAR INFUSIONS OF HYPERTONIC SALT IN RATS
SYMPATHETIC HYPERACTIVITY ELEVATES BLOOD-PRESSURE DURING ACUTE CEREBROVENTRICULAR INFUSIONS OF HYPERTONIC SALT IN RATS
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DOI：
10.1097/00005344-198409000-00017
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发表时间：
1984-01-01
影响因子：
3
通讯作者：
MIYAJIMA, E
中科院分区：
文献类型：
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作者：
BUNAG, RD;MIYAJIMA, E
将0.3 M NaCl的高渗溶液注入麻醉大鼠的第三脑室（ICV）20分钟，使平均主动脉压持续升高约10 mm Hg。心率和交感神经活动在最初几分钟内略有下降，但随后加速达到高于输注前水平。相比之下，ICV输注无效; 0.6 M尿素轻微降压，而0.3 M氯化铵升高血压，而不影响交感神经活动。在大鼠预处理与加压素拮抗剂，早期高渗氯化钠升压作用被抑制，而交感神经放电，而不是最初被抑制，增加从一开始。在ICV输注的前5分钟期间发生的血压升高被认为部分是由于内源性加压素分泌增加引起的血管收缩，并且在前10分钟之后随后的血压升高维持归因于交感神经过度活跃。由于加压和交感神经反应大大增强后，双侧迷走神经切断术或窦主动脉去神经，它被认为是在完整的大鼠高渗氯化钠的反应抑制心肺和窦主动脉压力感受器传入。压力感受器传入通路中断后升压反应的增强表明，高渗NaCl产生的交感神经活动和血压的增加可能有助于盐诱导的高血压，特别是当压力感受器缓冲不足时。
Hypertonic solutions of 0.3 M NaCl infused into the 3rd ventricle (ICV) for 20 min in urethane-anesthetized rats consistently elevated mean aortic pressure by about 10 mm Hg. Heart rate and sympathetic nerve activity diminished slightly during the first few minutes but then accelerated to attain higher than preinfusion levels. By contrast, ICV infusions were ineffective; 0.6 M urea were slightly depressor, while 0.3 M ammonium chloride elevated blood pressure without affecting sympathetic nerve activity. In rats pretreated with a vasopressin antagonist, the early hypertonic NaCl pressor effects were inhibited, while sympathetic nerve firing, instead of being initially inhibited, increased from the onset. The blood pressure elevation occurring during the first 5 min of ICV infusion was considered partly due to vasoconstriction caused by increased endogenous vasopressin secretion and subsequent blood pressure elevation maintenance after the first 10 in was attributed to sympathetic overactivity. Because pressor and sympathetic nerve responses were substantially enhanced following bilateral vagotomy or sinoaortic denervation, it was considered that responsiveness to hypertonic NaCl in intact rats is inhibited by both cardiopulmonary and sinoaortic baroreceptor afferents. Augmentation of pressor responsiveness following baroreceptor afferent pathway interruption suggests that increases in sympathetic activity and blood pressure produced by hypertonic NaCl could contribute to salt-induced hypertension, particularly when baroreceptor buffering becomes deficient.