Grassi G, Cattaneo B M, Seravalle G, Lanfranchi A, Bolla G, Mancia G
Cattedra di Medicina Interna, Ospedale S. Gerardo, Monza, Universita di Milano, Milan, Italy.
Hypertension. 1997 Mar;29(3):802-7. doi: 10.1161/01.hyp.29.3.802.
Low sodium intake is the most widely used nonpharmacological approach to the treatment of hypertension. Although nonpharmacological treatment is by definition regarded as safe, the suggestion has been made that low sodium intake is not totally devoid of inconveniences, and animal data have shown it to be accompanied by an impairment of reflex blood pressure control and homeostasis. However, no data exist on this issue in humans. In mild essential hypertensive patients (age, 34.1+/-3.3 years [mean+/-SEM]), we measured beat-to-beat arterial blood pressure (finger photoplethysmographic device), heart rate (electrocardiogram), and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor stimulation and deactivation, induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Measurements were performed at the end of three dietary periods, ie, after 8 days of regular sodium intake (210 mmol NaCl/d), low sodium intake (20 mmol NaCl/d) with unchanged potassium intake, and again regular sodium intake. Compared with the initial regular sodium diet, low sodium intake reduced urinary sodium excretion, whereas urinary potassium excretion was unchanged. Systolic blood pressure was significantly (P<.05), although slightly, reduced, whereas diastolic blood pressure was unaffected. Muscle sympathetic nerve activity was increased by 23.1+/-5.2% (P<.05). The increase was accompanied by a clear-cut impairment of the baroreceptor ability to modulate muscle sympathetic nerve activity, ie, by a 43.9+/-5.7% (P<.01) reduction in the sensitivity of the baroreceptor-muscle sympathetic nerve activity reflex compared with the control condition. Baroreceptor modulation of heart rate was also impaired, although to a smaller and less consistent extent. When regular sodium intake was restored, all the above-mentioned parameters and baroreflex responses returned to the values observed at the initial regular sodium diet. These data raise evidence that in humans sodium restriction may impair the arterial baroreflex. This may be responsible for the sympathetic activation occurring in this condition and for the impairment of blood pressure homeostasis.
低钠摄入是治疗高血压最广泛使用的非药物方法。虽然从定义上讲非药物治疗被认为是安全的，但有人提出低钠摄入并非完全没有不便之处，动物数据表明它会伴随着反射性血压控制和体内平衡的损害。然而，在人类中尚无关于此问题的数据。在轻度原发性高血压患者（年龄，34.1±3.3岁[平均值±标准误]）中，我们在静息状态以及分别通过静脉逐步输注去氧肾上腺素和硝普钠诱导的压力感受器刺激和失活期间，测量了逐搏动脉血压（手指光电容积描记装置）、心率（心电图）和节后肌肉交感神经传出活动（微神经ography）。在三个饮食阶段结束时进行测量，即常规钠摄入（210 mmol氯化钠/天）8天后、钾摄入量不变的低钠摄入（20 mmol氯化钠/天）后以及再次常规钠摄入后。与初始常规钠饮食相比，低钠摄入减少了尿钠排泄，而尿钾排泄未变。收缩压虽有显著降低（P<0.05），但幅度较小，而舒张压未受影响。肌肉交感神经活动增加了23.1±5.2%（P<0.05）。这种增加伴随着压力感受器调节肌肉交感神经活动能力的明显损害，即与对照状态相比，压力感受器 - 肌肉交感神经活动反射的敏感性降低了43.9±5.7%（P<0.01）。压力感受器对心率的调节也受到损害，尽管程度较小且不太一致。当恢复常规钠摄入时，上述所有参数和压力反射反应均恢复到初始常规钠饮食时观察到的值。这些数据证明，在人类中，钠限制可能会损害动脉压力反射。这可能是这种情况下发生交感神经激活以及血压稳态受损的原因。
