Peng N, Meng Q C, Oparil S, Wyss J M
Department of Cell Biology, University of Alabama at Birmingham, 35294-0019, USA.
Hypertension. 1996 Mar;27(3 Pt 2):578-83. doi: 10.1161/01.hyp.27.3.578.
Ingestion of a high NaCl diet elevates arterial pressure in spontaneously hypertensive rats, at least in part, by reducing the release of norepinephrine in the anterior hypothalamic area. The mechanism by which dietary NaCl excess alters anterior hypothalamic area norepinephrine release is unknown. Plasma Na+ is slightly elevated after ingestion of a meal; therefore, in the present study we tested the hypothesis that a small increase in plasma Na+ could reduce the release of norepinephrine in the anterior hypothalamic area and elevate arterial pressure. Male spontaneously hypertensive rats were randomized to be fed a diet containing either 1% (basal) or 8% (high) NaCl at age 7 weeks and were maintained on the diets for 2 weeks. Age-matched normotensive Wistar-Kyoto rats received a basal NaCl diet only. All rats were instrumented with a push/pull cannula, and 5 days later, the baseline release of 3-methoxy-4-hydroxyphenyl glycol (the major metabolite of norepinephrine in brain) was measured in awake, freely moving rats. Rats were then challenged with an intravenous infusion (75 microL/min) of hypertonic (2.7%) saline for 20 minutes. In spontaneously hypertensive rats fed a basal NaCl diet, the hypertonic saline infusion elevated mean arterial pressure by 12% and reduced the concentration of the norepinephrine metabolite in the anterior hypothalamic area by 19%; these alterations persisted after termination of the hypertonic saline infusion. Spontaneously hypertensive rats maintained on the high NaCl diet showed greatly reduced arterial pressure and norepinephrine metabolite responses. In normotensive control rats compared with the hypertensive rats fed the basal NaCl diet, the hypertonic saline had considerably less effects on arterial pressure and norepinephrine metabolite levels in the anterior hypothalamic area, and the responses were significantly shorter. Thus, a small elevation in plasma Na+ can reduce the release of norepinephrine in the anterior hypothalamic area. This response is greatly exaggerated in spontaneously hypertensive rats fed a basal (but not a high) NaCl diet, suggesting that a postprandial rise in NaCl could initiate the fall in norepinephrine and thereby contribute to the rise in arterial pressure in spontaneously hypertensive rats ingesting a high NaCl diet.
摄入高盐饮食会使自发性高血压大鼠的动脉血压升高，至少部分原因是减少了下丘脑前部区域去甲肾上腺素的释放。饮食中过量的氯化钠改变下丘脑前部区域去甲肾上腺素释放的机制尚不清楚。进食后血浆Na⁺会略有升高；因此，在本研究中，我们检验了以下假设：血浆Na⁺的小幅升高会减少下丘脑前部区域去甲肾上腺素的释放并升高动脉血压。雄性自发性高血压大鼠在7周龄时被随机分为两组，分别喂食含1%（基础）或8%（高）氯化钠的饮食，并维持2周。年龄匹配的正常血压Wistar-Kyoto大鼠仅接受基础氯化钠饮食。所有大鼠均安装了推挽式套管，5天后，在清醒、自由活动的大鼠中测量3-甲氧基-4-羟基苯乙二醇（脑中去甲肾上腺素的主要代谢产物）的基线释放量。然后，大鼠接受静脉输注（75微升/分钟）高渗（2.7%）盐水20分钟。在喂食基础氯化钠饮食的自发性高血压大鼠中，高渗盐水输注使平均动脉血压升高了12%，并使下丘脑前部区域去甲肾上腺素代谢产物的浓度降低了19%；高渗盐水输注终止后，这些改变仍然存在。维持高盐饮食的自发性高血压大鼠的动脉血压和去甲肾上腺素代谢产物反应大大降低。与喂食基础氯化钠饮食的高血压大鼠相比，正常血压对照大鼠中，高渗盐水对动脉血压和下丘脑前部区域去甲肾上腺素代谢产物水平的影响要小得多，且反应明显更短。因此，血浆Na⁺的小幅升高会减少下丘脑前部区域去甲肾上腺素的释放。在喂食基础（而非高）氯化钠饮食的自发性高血压大鼠中，这种反应被大大夸大，这表明餐后氯化钠的升高可能引发去甲肾上腺素的下降，从而导致摄入高盐饮食的自发性高血压大鼠动脉血压升高。
