Dornfeld L P, Maxwell M H, Waks A, Tuck M
School of Medicine University of California, Los Angeles 90024.
Kidney Int Suppl. 1987 Oct;22:S254-8.
We conclude that the following may explain the rise in blood pressure with obesity and the subsequent fall in blood pressure (Fig. 2): (1) An increase in calories, protein, or carbohydrate leads to an increase in plasma catecholamines, sympathetic nervous system activity, and insulin secretion. (2) These factors, in turn, lead to increased renal sodium retention and stimulation of the renin-aldosterone system which, in turn, leads to: (3) An increased cardiac output with an inability to appropriately adjust the peripheral resistance to maintain normotension with resultant hypertension. Conversely, the fall in blood pressure with weight reduction can be explained by (Fig. 3): (1) A decrease in calorie, carbohydrate, or protein intake which leads to: (2) A decrease in circulating plasma catecholamines, sympathetic nervous system activity, and insulin secretion which results in: (3) A natriuresis and decrease in the renin-aldosterone system, which causes a decrease in circulating blood volume and in cardiac output. This, in turn, lowers blood pressure towards normal. The unanswered question still remains: why do some obese patients become hypertensive and others remain normotensive? Perhaps there are weight-sensitive individuals and weight-resistant individuals just as there appear to be salt-sensitive and salt-resistant hypertensive patients. Perhaps the answer is genetic. These questions also remain to be answered.
我们得出结论，以下因素可能解释肥胖导致的血压升高以及随后的血压下降（图2）：（1）热量、蛋白质或碳水化合物的增加会导致血浆儿茶酚胺、交感神经系统活动和胰岛素分泌增加。（2）这些因素进而导致肾脏钠潴留增加，并刺激肾素-醛固酮系统，这反过来又会导致：（3）心输出量增加，但无法适当调节外周阻力以维持正常血压，从而导致高血压。相反，体重减轻导致的血压下降可以用（图3）来解释：（1）热量、碳水化合物或蛋白质摄入量减少，这会导致：（2）循环血浆儿茶酚胺、交感神经系统活动和胰岛素分泌减少，进而导致：（3）利钠作用以及肾素-醛固酮系统减弱，这会导致循环血容量和心输出量减少。这反过来会使血压降至正常水平。尚未解决的问题仍然存在：为什么一些肥胖患者会患高血压而另一些人仍保持正常血压？也许存在体重敏感个体和体重抵抗个体，就像似乎存在盐敏感和盐抵抗高血压患者一样。也许答案是遗传因素。这些问题仍有待解答。
