Krishna G G, Kapoor S C
Temple University, Philadelphia, Pennsylvania.
Ann Intern Med. 1991 Jul 15;115(2):77-83. doi: 10.7326/0003-4819-115-2-77.
To determine the effect of potassium depletion on blood pressure in patients with essential hypertension.
Double-blind, randomized, crossover study, with each patient serving as his or her own control.
Clinical research center at a university hospital.
Twelve patients with hypertension.
Patients were placed on 10-day isocaloric diets providing a daily potassium intake of either 16 mmol or 96 mmol. The intake of sodium (120 mmol/d) and other minerals was kept constant. On day 11 each patient received a 2-litre isotonic saline infusion over 4 hours.
Blood pressure; urinary excretion rates for sodium, potassium, calcium, and phosphorous; glomerular filtration rate; renal plasma flow; and plasma levels of vasoactive hormones.
With low potassium intake, systolic blood pressure increased (P = 0.01) by 7 mm Hg (95% CI, 3 mm Hg to 11 mm Hg) and diastolic pressure increased (P = 0.04) by 6 mm Hg (CI, 1 mm Hg to 11 mm Hg), whereas plasma potassium concentration decreased (P less than 0.001) by 0.8 mmol/L (CI, 0.4 to 1.0 mmol/L). In response to a 2-litre isotonic saline infusion, the mean arterial pressure increased similarly on both diets but reached higher levels on low potassium intake (115 +/- 2 mm Hg compared with 109 +/- 2 mm Hg, P = 0.03). Potassium depletion was associated with a decrease in sodium excretion (83 +/- 6 mmol/d compared with 110 +/- 5 mmol/d, P less than 0.001). Plasma renin activity and plasma aldosterone concentrations also decreased in patients during low potassium intake, but concentrations of arginine vasopressin and atrial natriuretic peptide, glomerular filtration rate, and renal plasma flow were unchanged. Further, low potassium intake increased urinary excretion of calcium and phosphorus and of plasma immunoreactive parathyroid hormone levels.
Dietary potassium restriction increases blood pressure in patients with essential hypertension. Both sodium retention and calcium depletion may contribute to the increase in blood pressure during potassium depletion.
确定钾缺乏对原发性高血压患者血压的影响。
双盲、随机、交叉研究，每位患者作为自身对照。
大学医院的临床研究中心。
12例高血压患者。
患者接受为期10天的等热量饮食，每日钾摄入量分别为16 mmol或96 mmol。钠（120 mmol/d）和其他矿物质的摄入量保持恒定。在第11天，每位患者在4小时内接受2升等渗盐水输注。
血压；钠、钾、钙和磷的尿排泄率；肾小球滤过率；肾血浆流量；以及血管活性激素的血浆水平。
低钾摄入时，收缩压升高（P = 0.01）7 mmHg（95%可信区间，3 mmHg至11 mmHg），舒张压升高（P = 0.04）6 mmHg（可信区间，1 mmHg至11 mmHg），而血浆钾浓度降低（P < 0.001）0.8 mmol/L（可信区间，0.4至1.0 mmol/L）。对2升等渗盐水输注的反应，两种饮食时平均动脉压升高相似，但低钾摄入时达到更高水平（115±2 mmHg对比109±2 mmHg，P = 0.03）。钾缺乏与钠排泄减少相关（83±6 mmol/d对比110±5 mmol/d，P < 0.001）。低钾摄入期间患者的血浆肾素活性和血浆醛固酮浓度也降低，但精氨酸加压素和心房利钠肽浓度、肾小球滤过率和肾血浆流量未改变。此外，低钾摄入增加了钙、磷的尿排泄以及血浆免疫反应性甲状旁腺激素水平。
饮食中钾限制会使原发性高血压患者血压升高。钠潴留和钙缺乏可能都促成了钾缺乏时血压的升高。
