Krishna G G, Kapoor S C
Renal Electrolyte Section, University of Pennsylvania, Philadelphia.
Kidney Int. 1993 May;43(5):1097-103. doi: 10.1038/ki.1993.154.
Potassium depletion induced by dietary potassium restriction causes sodium retention while potassium supplementation augments urinary sodium excretion. The role of external potassium balance in modulating mineralocorticoid-induced sodium retention in humans is unknown. Accordingly, eight healthy subjects were studied at the Clinical Research Center receiving a constant diet providing (per kg body wt) sodium 2.5 mmol, potassium 1.1 mmol daily. After establishing basal sodium and potassium balance over three days, each subject received 9 alpha-fludrocortisone 0.4 mg/day for 10 days. Subjects were studied twice, four to eight weeks apart, in a double blind, randomized crossover design receiving either placebo or additional KCl (80 mmol/day) over the 10 day study period. Serum potassium concentrations were unchanged from basal values on KCl while the values fell (4.1 +/- 0.1 vs. 3.4 +/- 0.1 mmol/liter, P = 0.01) on placebo. Urinary sodium excretion decreased with fludrocortisone administration in both groups, but this decrease reached significance only in the placebo group. Furthermore, during fludrocortisone administration the sodium excretion rates on KCl were significantly higher compared to the values noted on placebo (134 +/- 8 vs. 112 +/- 13 mmol/day, P = 0.01). Body weight recorded after 10 days of fludrocortisone administration was higher on placebo compared to KCl (72.3 +/- 2.8 vs. 71.6 +/- 2.8 kg, P = 0.01). Plasma renin activity, and aldosterone concentrations decreased on fludrocortisone while atrial natriuretic peptide levels increased. These studies suggest that amelioration of hypokalemia attenuates mineralocorticoid-induced sodium retention. Therefore, potassium depletion may contribute to the mineralocorticoid-induced sodium retention.
饮食中钾限制诱导的钾缺乏会导致钠潴留，而补充钾则会增加尿钠排泄。外部钾平衡在调节人体盐皮质激素诱导的钠潴留中的作用尚不清楚。因此，在临床研究中心对八名健康受试者进行了研究，他们接受恒定饮食，每天提供（每千克体重）2.5 mmol钠、1.1 mmol钾。在三天内建立基础钠和钾平衡后，每位受试者每天接受0.4 mg 9α-氟氢可的松，持续10天。受试者在双盲、随机交叉设计中接受两次研究，间隔四至八周，在为期10天的研究期间接受安慰剂或额外的氯化钾（80 mmol/天）。氯化钾组的血清钾浓度与基础值相比无变化，而安慰剂组的值下降（4.1±0.1对3.4±0.1 mmol/升，P = 0.01）。两组中，氟氢可的松给药后尿钠排泄均减少，但仅在安慰剂组中这种减少具有统计学意义。此外，在氟氢可的松给药期间，氯化钾组的钠排泄率显著高于安慰剂组（134±8对112±13 mmol/天，P = 0.01）。氟氢可的松给药10天后记录的体重，安慰剂组高于氯化钾组（72.3±2.8对71.6±2.8 kg，P = 0.01）。氟氢可的松给药后血浆肾素活性和醛固酮浓度降低，而心房利钠肽水平升高。这些研究表明，低钾血症的改善可减轻盐皮质激素诱导的钠潴留。因此，钾缺乏可能导致盐皮质激素诱导的钠潴留。
