Mark A L, Lawton W J, Abboud F M, Fitz A E, Connor W E, Heistad D D
Circ Res. 1975 Jun;36(6 Suppl 1):194-8. doi: 10.1161/01.res.36.6.194.
The purpose of this study was to evaluate effects of high and low sodium intake on arterial pressure and forearm vascular resistance in subjects with borderline hypertension and to compare responses to sodium excess in these subjects with responses in a recent study in normotensive subjects. Six subjects with borderline hypertension were studied after ten days of high (410 mEq/24hr) and low (10mEq/24hr) sodium intake. Potassium intake was constant. In five of six subjects, high sodium intake decreased forearm blood flow and increased forearm vascular resistance and arterial pressure. During low and high sodium intake forearm blood flow averaged 7.8 plus or minus 1.2 (SE) and 5.9 plus or minus 0.8 ml/min x 100 ml, respectively; forearm vascular resistance averaged 13.5 plus or minus 2.2 and 19.1 plus or minus 3.0 units, respectively; and mean arterial pressure averaged 89 plus or minus 3 and 98 plus or minus 2 mm Hg, respectively. High sodium intake augmented forearm vasoconstrictor responses to lower body negative pressure, a stimulus to neurogenic vasoconstriction. The results contrast with our earlier results in normotensive subjects in whom sodium excess produced forearm vasodilatation and failed to increase arterial pressure significantly. Decreases in renin and aldosterone with high sodium intake were similar in the two groups. The results suggest that excessive sodium intake in subjects with borderline hypertension produces abnormal increases in forearm vascular resistance, neurogenic vasoconstriction, and arterial pressure. The reasons for the contrast between the borderline hypertensives and normotensives are unknown, but they do not seem to be related to the renin-angiotensin-aldosterone system.
本研究的目的是评估高钠和低钠摄入对临界高血压患者动脉压和前臂血管阻力的影响，并将这些患者对钠过量的反应与近期一项针对正常血压受试者的研究中的反应进行比较。对6名临界高血压患者在高钠（410 mEq/24小时）和低钠（10 mEq/24小时）摄入10天后进行了研究。钾的摄入量保持恒定。在6名受试者中的5名中，高钠摄入降低了前臂血流量，增加了前臂血管阻力和动脉压。在低钠和高钠摄入期间，前臂血流量平均分别为7.8±1.2（标准误）和5.9±0.8 ml/min x 100 ml；前臂血管阻力平均分别为13.5±2.2和19.1±3.0单位；平均动脉压平均分别为89±3和98±2 mmHg。高钠摄入增强了前臂血管对下体负压的收缩反应，下体负压是一种神经源性血管收缩的刺激因素。这些结果与我们早期在正常血压受试者中的结果形成对比，在正常血压受试者中，钠过量导致前臂血管扩张且未能显著增加动脉压。两组中高钠摄入时肾素和醛固酮的降低情况相似。结果表明，临界高血压患者过量摄入钠会导致前臂血管阻力、神经源性血管收缩和动脉压异常升高。临界高血压患者与正常血压患者之间存在差异的原因尚不清楚，但似乎与肾素 - 血管紧张素 - 醛固酮系统无关。
