Clin Exp Hypertens A. 1989;11(5-6):1011-24. doi: 10.3109/10641968909035388.
Eighty-eight untreated subjects (mean age 58.6 +/- 1.1 years; 73 males and 15 females) with diastolic blood pressure between 90 and 100 mmHg were recruited to the study. Subjects were seen fortnightly and after four pre-diet visits were randomised into a normal sodium intake group (44 subjects receiving less than 80 mmol sodium daily in the diet plus 80 mmol of sodium supplement as eight slow release sodium chloride tablets daily) or a low sodium intake group (44 subjects receiving less than 80 mmol sodium daily in the diet plus eight slow release sodium chloride placebo tablets daily). Eight weeks later, subjects crossed over to the alternate tablets while continuing with the reduced sodium diet for another period of 8 weeks. The difference in urine sodium between the low sodium phase and the normal sodium phase was 67 +/- 4 mmol/day independent of the order in which the treatments were given; the corresponding difference in urine potassium excretion was 1.2 +/- 1.4 mmol/day and was not significant. The differences in systolic and diastolic blood pressures between the low sodium and normal sodium phases for all 88 subjects were 3.6 +/- 0.7 mmHg (95% confidence intervals 2.2-5.0) and 2.1 +/- 0.4 mmHg (95% confidence intervals 1.3-2.9) respectively, and were independent of the order in which treatments were given (p less than 0.005). On the other hand, comparison of the blood pressures of the two cohorts of subjects as parallel groups during the first test phase revealed that the falls in pressure were greater by 5.3 +/- 1.4 (95% confidence intervals 2.7-8.1) mmHg (systolic) and 3.4 +/- 0.8 (95% confidence intervals 1.8-5.0) mmHg (diastolic) in subjects with low sodium intake compared with those with normal sodium intake. These differences in blood pressure reduction obtained by analysis of the crossover study and of the parallel group study were not significant, with clear overlap of the 95% confidence intervals. Moderate dietary salt restriction causes reductions in blood pressure and around 3.5-5.5 mmHg (systolic) and 2-3.5 mmHg (diastolic) of these falls can be attributed specifically to reduction of sodium chloride intake.
88名未经治疗的受试者（平均年龄58.6±1.1岁；73名男性和15名女性），舒张压在90至100 mmHg之间，被招募进入该研究。受试者每两周接受一次检查，在进行四次饮食前检查后，被随机分为正常钠摄入组（44名受试者，饮食中每日钠摄入量少于80 mmol，外加每日八片缓释氯化钠片补充80 mmol钠）或低钠摄入组（44名受试者，饮食中每日钠摄入量少于80 mmol，外加每日八片缓释氯化钠安慰剂片）。八周后，受试者交叉服用另一种片剂，同时继续低钠饮食8周。低钠阶段和正常钠阶段之间尿钠的差异为67±4 mmol/天，与治疗顺序无关；尿钾排泄的相应差异为1.2±1.4 mmol/天，无统计学意义。88名受试者在低钠阶段和正常钠阶段的收缩压和舒张压差异分别为3.6±0.7 mmHg（95%置信区间2.2 - 5.0）和2.1±0.4 mmHg（95%置信区间1.3 - 2.9），且与治疗顺序无关（p<0.005）。另一方面，在第一个测试阶段，将两组受试者作为平行组进行血压比较发现，与正常钠摄入的受试者相比，低钠摄入的受试者收缩压下降幅度更大，为5.3±1.4（95%置信区间2.7 - 8.1）mmHg，舒张压下降幅度更大，为3.4±0.8（95%置信区间1.8 - 5.0）mmHg。通过交叉研究和平行组研究分析得到的血压降低差异无统计学意义，95%置信区间明显重叠。适度的饮食盐限制可导致血压降低，其中约3.5 - 5.5 mmHg（收缩压）和2 - 3.5 mmHg（舒张压）的降低可具体归因于氯化钠摄入量的减少。
