Pratt J H, Manatunga A K, Hanna M P, Ambrosius W T
Department of Medicine, Indiana University School of Medicine and the Veterans Administration Medical Center, Indianapolis, USA.
J Hypertens. 1997 Aug;15(8):877-83. doi: 10.1097/00004872-199715080-00012.
We had observed previously that the aldosterone excretion rate and plasma aldosterone concentration were lower for black children than they were for white children. We did not know whether this was secondary to a lower intake of potassium or to suppression of the renin-angiotensin system in blacks.
To test the hypothesis that the secretion of aldosterone in response to potassium would be different in blacks than in a control group of whites.
Black and white subjects were selected on the basis of their having aldosterone excretion rates that were in the lowest quartile for the entire original cohort. Since the blacks typically had lower aldosterone excretion rates than did the whites, the black participants were represented primarily by those with average rates of aldosterone production among blacks, whereas the whites were represented by those with the lowest aldosterone production rates among whites. The protocol consisted of a placebo-controlled, randomized cross-over study design.
Twelve blacks and 12 whites, aged 14.1 +/- 1.6 (mean +/- SD) and 15.4 +/- 2.1 years, respectively, were allocated randomly to double-blind treatment either with placebo or with 40 mmol/day potassium chloride for 7 days and then the alternate treatment Measurements of the plasma renin activity (PRA), plasma aldosterone concentration, and urinary aldosterone excretion were performed in an inpatient research unit at the end of the treatment. The blood pressure was monitored for 24 h.
Treatment with potassium increased the plasma aldosterone concentration (P = 0.0006) and the urinary excretion of aldosterone (P = 0.0002) significantly both for blacks and for whites. There was no significant racial difference in the response to potassium. The PRA was overall 1.605-fold lower in the blacks than it was in the whites (P = 0.0124). The lowest PRA levels, such as those in the blacks when they were supine, tended to be increased with the potassium treatment. The blood pressure did not change significantly with the potassium supplement for either racial group.
After we had supplemented the intake of potassium, aldosterone production increased in the blacks and in the control group of whites to the same extent The potassium treatment appeared to increase lower PRA levels. A lower intake of potassium could at least partially account for the suppression of the renin-aldosterone system in blacks.
我们之前观察到，黑人儿童的醛固酮排泄率和血浆醛固酮浓度低于白人儿童。我们不知道这是由于黑人钾摄入量较低，还是由于黑人肾素 - 血管紧张素系统受到抑制。
检验黑人对钾反应时醛固酮分泌与白人对照组不同的假设。
根据醛固酮排泄率处于整个原始队列最低四分位数来选择黑人和白人受试者。由于黑人的醛固酮排泄率通常低于白人，黑人参与者主要由黑人中醛固酮产生平均速率的个体代表，而白人则由白人中醛固酮产生速率最低的个体代表。方案采用安慰剂对照、随机交叉研究设计。
12名黑人和12名白人，年龄分别为14.1±1.6（均值±标准差）岁和15.4±2.1岁，被随机分配接受双盲治疗，要么服用安慰剂，要么服用40 mmol/天氯化钾，为期7天，然后交替治疗。在治疗结束时，于住院研究单元测量血浆肾素活性（PRA）、血浆醛固酮浓度和尿醛固酮排泄量。监测24小时血压。
钾治疗使黑人和白人的血浆醛固酮浓度（P = 0.0006）和醛固酮尿排泄量（P = 0.0002）均显著增加。对钾的反应没有显著种族差异。黑人的PRA总体上比白人低1.605倍（P = 0.0124）。最低的PRA水平，如黑人仰卧时的水平，在钾治疗后趋于升高。两个种族组补充钾后血压均无显著变化。
补充钾摄入后，黑人和白人对照组的醛固酮产生增加程度相同。钾治疗似乎使较低的PRA水平升高。钾摄入量较低至少可以部分解释黑人肾素 - 醛固酮系统受到抑制的原因。
