Lee L C, Sasaki S, Inoue A, Fukuyama M, Nakamura Y, Oguro M, Kawasaki S, Hayashi J, Takeda K, Yoshimura M
Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
J Cardiovasc Pharmacol. 1988 Aug;12(2):179-85. doi: 10.1097/00005344-198808000-00008.
Tail-cuff systolic pressures became elevated in male Wistar rats fed chow containing 8% NaCl for 4 weeks. After 4 weeks of salt loading, pressor and sympathetic responses to ventromedial hypothalamic stimulation were larger in salt-loaded rats. When similar experiments were done following sinoaortic denervation, all of the effects previously induced by dietary salt loading persisted. By contrast, after only 1 week of salt loading, pressor and sympathetic responses to hypothalamic stimulation were reduced, instead of being increased. Since circulating plasma volume was increased in week 1, it was considered possible that reduced hypothalamic responsiveness was due to enhanced cardiopulmonary baroreflexes. Supporting this interpretation, bilateral vagotomy reversed the hypothalamic inhibition occurring in week 1. Although neither the site nor mechanism causing sympathetic hyperactivity has been determined, our results indicate that chronic dietary salt loading has biphasic effects on the ventromedial hypothalamus: an initial inhibition in the first week followed by stimulation thereafter. These results could mean that dietary salt loading eventually increases sympathetic activity and thereby induces hypertension by stimulating the ventromedial hypothalamus.
给雄性Wistar大鼠喂食含8%氯化钠的饲料4周后，尾套法测量的收缩压升高。在高盐饮食4周后，高盐负荷大鼠对下丘脑腹内侧刺激的升压反应和交感反应更大。当在去窦主动脉神经后进行类似实验时，先前由饮食盐负荷诱导的所有效应都持续存在。相比之下，仅在高盐饮食1周后，对下丘脑刺激的升压反应和交感反应反而降低，而非增加。由于第1周时循环血浆量增加，因此认为下丘脑反应性降低可能是由于心肺压力反射增强所致。双侧迷走神经切断术逆转了第1周出现的下丘脑抑制，支持了这一解释。虽然导致交感神经过度活跃的部位和机制尚未确定，但我们的结果表明，慢性饮食盐负荷对下丘脑腹内侧有双相作用：第1周出现初始抑制，随后是刺激。这些结果可能意味着饮食盐负荷最终会增加交感神经活动，从而通过刺激下丘脑腹内侧诱发高血压。
