Franzoni F, Santoro G, Carpi A, Da Prato F, Bartolomucci F, Femia F R, Prattichizzo F, Galetta F
Department of Internal Medicine, University of Pisa School of Medicine, via Roma 67, 56126 Pisa, Italy.
Biomed Pharmacother. 2005 Jan-Feb;59(1-2):25-9. doi: 10.1016/j.biopha.2004.11.002. Epub 2005 Jan 20.
Previous studies showed that potassium chloride (48-120 mmol/day) supplementation reduced arterial blood pressure (BP) in hypertensive patients.
Our aim was to evaluate the effect of a lower dose of potassium aspartate salt on BP in individuals with essential arterial hypertension.
One hundred and four patients (65 males, age 53 +/- 12 years) with mild to moderate essential hypertension (systolic/diastolic BP 154.2/96.2 +/- 10.8/5.4 mmHg) were allocated in two comparable groups of 52 to receive or not 30 mmol/day per os of potassium aspartate supplementation for four weeks. Office and 24-h BP, as well as serum and urinary electrolytes, were measured at baseline and at the follow-up visit after four weeks.
Office and 24-h BP did not change in the control group, while these values were significantly reduced in the potassium supplementation group. Changes in office (systolic BP: 154.4 +/- 8.2 vs. 142.2 +/- 7.6 mmHg; diastolic BP: 95.0 +/- 5.6 vs. 87.2 +/- 4.3 mmHg, P < 0.001 for both) and 24-h BP (systolic BP: 142.7 +/- 8.2 vs. 134.8 +/- 6.3 mmHg; diastolic BP: 90.8 +/- 4.4 vs. 84.6 +/- 3.8 mmHg, P < 0.001 for both) following potassium supplementation were highly significant. The changes in day time and night time BP were similar. The treated group showed significantly increased potassium serum level and 24-h urinary excretion of potassium (P < 0.01 in both cases) after four weeks, while the untreated group showed no significant changes of the same parameters. Urinary Na/K ratio decreased significantly with potassium supplementation (P < 0.001). In the treated group changes in office (r = 0.58, P < 0.001) and 24-h SBP (r = 0.51, P < 0.001), but not in DBP (r = 0.29 and r = 0.25, n.s.), correlated positively with the urinary Na/K ratio at baseline.
A relatively low supplementation of 30 mmol/day of potassium as aspartate lowered office and 24-h ambulatory BP in subjects with mild to moderate essential hypertension. The antihypertensive effect was sustained throughout the day, and was greater in the patients with high basal urinary Na/K ratio.
既往研究表明，补充氯化钾（48 - 120 mmol/天）可降低高血压患者的动脉血压（BP）。
我们的目的是评估较低剂量的门冬氨酸钾盐对原发性高血压患者血压的影响。
104例患者（65例男性，年龄53±12岁）患有轻度至中度原发性高血压（收缩压/舒张压BP 154.2/96.2±10.8/5.4 mmHg），被分为两组，每组52例，一组口服30 mmol/天门冬氨酸钾补充剂四周，另一组不补充。在基线和四周后的随访时测量诊室血压和24小时血压，以及血清和尿液电解质。
对照组的诊室血压和24小时血压未发生变化，而补充钾组的这些值显著降低。补充钾后诊室血压（收缩压：154.4±8.2 vs. 142.2±7.6 mmHg；舒张压：95.0±5.6 vs. 87.2±4.3 mmHg，两者P<0.001）和24小时血压（收缩压：142.7±8.2 vs. 134.8±6.3 mmHg；舒张压：90.8±4.4 vs. 84.6±3.8 mmHg，两者P<0.001）的变化非常显著。白天和夜间血压的变化相似。四周后，治疗组血清钾水平和24小时尿钾排泄量显著增加（两者P<0.01），而未治疗组这些参数无显著变化。补充钾后尿钠/钾比值显著降低（P<0.001）。在治疗组中，诊室血压（r = 0.58，P<0.001）和24小时收缩压（r = 0.51，P<0.001）的变化与基线时的尿钠/钾比值呈正相关，但舒张压（r = 0.29和r = 0.25，无统计学意义）与基线时的尿钠/钾比值无相关性。
每天相对低剂量补充30 mmol的门冬氨酸钾可降低轻度至中度原发性高血压患者的诊室血压和24小时动态血压。降压作用全天持续，在基础尿钠/钾比值高的患者中降压作用更强。
