Sasaki S, Buñag R D
Am J Physiol. 1983 Jun;244(6):R751-7. doi: 10.1152/ajpregu.1983.244.6.R751.
In rats made to drink isotonic saline solution instead of water for 5 wk, systolic pressure and heart rate, whether recorded indirectly from the tail or directly from femoral catheters, rose slightly. When the ventromedial hypothalamus was stimulated electrically, increases in arterial pressure and sympathetic neural firing were larger in saline-drinking than in water-drinking rats. By contrast, pressor responses to injections of norepinephrine or tyramine were unaltered. Following bilateral destruction of the ventromedial hypothalamus in other rats, none of the effects of chronic saline ingestion was elicited. Although neither the site nor the mechanism causing sympathetic overactivity has been determined, our results are in accord with the interpretation that salt loading elevates blood pressure, at least in part, by stimulating the ventromedial hypothalamus to increase sympathetic activity.
让大鼠饮用等渗盐溶液而非水达5周，无论通过间接测量尾部还是直接从股动脉导管记录，其收缩压和心率均略有上升。当对腹内侧下丘脑进行电刺激时，饮用盐水的大鼠动脉压升高幅度及交感神经放电增加幅度比饮用纯水的大鼠更大。相比之下，注射去甲肾上腺素或酪胺引起的升压反应未发生改变。在其他大鼠双侧损毁腹内侧下丘脑后，未引发慢性摄入盐水的任何效应。尽管导致交感神经过度活跃的部位和机制均未明确，但我们的结果符合这样的解释：盐负荷至少部分通过刺激腹内侧下丘脑增加交感神经活动来升高血压。
