Sharma A M, Kribben A, Schattenfroh S, Cetto C, Distler A
Department of General Internal Medicine and Nephrology, Universitätsklinikum Steglitz, Free University of Berlin, FRG.
Hypertension. 1990 Oct;16(4):407-13. doi: 10.1161/01.hyp.16.4.407.
Metabolic acidosis has recently been observed in rat models of salt-sensitive genetic hypertension. To test the hypothesis that salt sensitivity in humans may be associated with abnormal acid-base homeostasis, we performed arterial blood gas analyses in young (20-31 years old) normotensive subjects (n = 40) who were placed on a low salt diet (20 mmol NaCl/day) for 2 weeks with either 200 mmol sodium chloride or placebo added to the low salt diet for 1 week each in a randomized, single-blind crossover order. Furthermore, a subset of the subjects (seven salt-sensitive and eight salt-resistant) received 200 mmol sodium/day as the citrate salt as a supplement to the low salt diet for a third week. During each regimen, blood pressure as well as arterial pH and bicarbonate levels were measured. Salt sensitivity was defined as a significant drop in mean arterial pressure greater than 3 mm Hg (mean of 30 readings taken during each diet, p less than 0.05) while the subject was on the low salt diet. According to this definition, 16 subjects were salt-sensitive and 24 salt-resistant. During the high sodium chloride regimen, arterial pH and bicarbonate levels were significantly lower in the salt-sensitive than in the salt-resistant group (p less than 0.0001). The increase in blood pressure caused by sodium chloride correlated inversely to the arterial pH (r = -0.57, p = 0.0002) and bicarbonate levels (r = -0.52, p = 0.0007) during the high salt diet. Sodium chloride increased mean arterial blood pressure in the salt-sensitive subjects; sodium citrate did not. Sodium citrate led to an increase in pH and bicarbonate levels in both groups. Our finding that a sodium chloride-induced rise in blood pressure is associated with lower arterial plasma pH and bicarbonate levels points to an abnormality in renal acid-base regulation in salt-sensitive subjects.
最近在盐敏感性遗传性高血压大鼠模型中观察到代谢性酸中毒。为了验证人类盐敏感性可能与酸碱稳态异常有关这一假设，我们对年轻（20 - 31岁）的血压正常受试者（n = 40）进行了动脉血气分析，这些受试者接受为期2周的低盐饮食（20 mmol氯化钠/天），然后按照随机、单盲交叉顺序，在低盐饮食中分别添加200 mmol氯化钠或安慰剂，各持续1周。此外，一部分受试者（7名盐敏感者和8名盐抵抗者）在第三周接受200 mmol柠檬酸钠盐作为低盐饮食的补充，每日摄入量为200 mmol。在每个方案期间，测量血压以及动脉pH值和碳酸氢盐水平。盐敏感性定义为在低盐饮食期间平均动脉压显著下降超过3 mmHg（每种饮食期间进行30次读数的平均值，p < 0.05）。根据这个定义，16名受试者为盐敏感者，24名受试者为盐抵抗者。在高氯化钠方案期间，盐敏感组的动脉pH值和碳酸氢盐水平显著低于盐抵抗组（p < 0.0001）。在高盐饮食期间，氯化钠引起的血压升高与动脉pH值（r = -0.57，p = 0.0002）和碳酸氢盐水平（r = -0.52，p = 0.0007）呈负相关。氯化钠使盐敏感受试者的平均动脉血压升高；柠檬酸钠则没有。柠檬酸钠使两组的pH值和碳酸氢盐水平都有所升高。我们的发现，即氯化钠引起的血压升高与较低的动脉血浆pH值和碳酸氢盐水平相关，表明盐敏感受试者存在肾酸碱调节异常。
