Suzuki H, Ikenaga H, Hayashida T, Otsuka K, Kanno Y, Ohno Y, Ikeda H, Saruta T
Second Department of Internal Medicine, Saitama Medical School, Japan.
Kidney Int Suppl. 1996 Jun;55:S150-3.
To investigate the role of sodium in obesity induced hypertension, Wistar fatty rats (WFR) were employed. This rat has the following characteristics: (1) hyperglycemia, (2) hyperinsulinemia, and (3) hypertriglycemia. Four percent sodium chloride with constant amount of food intake was administered to these rats from 8 to 16 weeks. During this period, body wt, food intake, water consumption, urine volume, systolic blood pressure, urinary excretion of sodium and potassium, urinary albumin excretion, plasma sodium and potassium, and plasma glucose and immunoreactive insulin (IRI) were measured before, and twice more during eight weeks. No remarkable changes were observed in plasma glucose level during these periods between the two groups. On the other hand, in group 1 IRI significantly increased compared with group 2. Mean blood pressure was increased from 110 +/- 5 to 130 +/- 8 mm Hg (P < 0.01). To ascertain whether this salt sensitivity relates to the abnormalities in pressure-natriuresis responses, the pressure-natriuresis (P-N) was characterized. The P-N curve in WFR was shifted to the right and its slope was flattened compared to its control Wistar lean rats. In conclusion, an excess of dietary sodium intake may contribute to an elevation of blood pressure in Wistar fatty rat with hyperglycemia and hyperinsulinemia. This salt sensitivity may change the abnormal pressure-natriuresis responses.
为研究钠在肥胖诱导的高血压中的作用，采用了Wistar肥胖大鼠（WFR）。这种大鼠具有以下特征：（1）高血糖，（2）高胰岛素血症，以及（3）高甘油三酯血症。从8周龄至16周龄，给这些大鼠喂食含4%氯化钠且食物摄入量恒定的饲料。在此期间，在8周内，分别于实验前及实验过程中另外两次测量大鼠的体重、食物摄入量、饮水量、尿量、收缩压、尿钠和钾排泄量、尿白蛋白排泄量、血浆钠和钾，以及血浆葡萄糖和免疫反应性胰岛素（IRI）。两组在这些时间段内血浆葡萄糖水平均未观察到显著变化。另一方面，与第2组相比，第1组的IRI显著升高。平均血压从110±5 mmHg升高至130±8 mmHg（P<0.01）。为确定这种盐敏感性是否与压力-利钠反应异常有关，对压力-利钠（P-N）进行了表征。与对照Wistar瘦大鼠相比，WFR的P-N曲线右移且斜率变平。总之，过量的膳食钠摄入可能导致伴有高血糖和高胰岛素血症的Wistar肥胖大鼠血压升高。这种盐敏感性可能改变异常的压力-利钠反应。
