To assess the effects of supplementation with oral potassium on blood pressure in humans.
Meta-analysis of randomized controlled trials.
English-language articles published before July 1995.
Thirty-three randomized controlled trials (2609 participants) in which potassium supplementation was the only difference between the intervention and control conditions.
Using a standardized protocol, 2 of us independently abstracted information on sample size, duration, study design, potassium dose, participant characteristics, and treatment results.
By means of a random-effects model, findings from individual trials were pooled, after results for each trial were weighted by the inverse of its variance. An extreme effect of potassium in lowering blood pressure was noted in 1 trial. After exclusion of this trial, potassium supplementation was associated with a significant reduction in mean (95% confidence interval) systolic and diastolic blood pressure of -3.11 mm Hg (-1.91 to -4.31 mm Hg) and -1.97 mm Hg (-0.52 to -3.42 mm Hg), respectively. Effects of treatment appeared to be enhanced in studies in which participants were concurrently exposed to a high intake of sodium.
Our results support the premise that low potassium intake may play an important role in the genesis of high blood pressure. Increased potassium intake should be considered as a recommendation for prevention and treatment of hypertension, especially in those who are unable to reduce their intake of sodium.
"Sodium excretion alone was not associated with AI however the sodium/potassium excretion ratio was indicating that the effect of diet on wave reflection appears to have been driven primarily by potassium intake in this group of subjects. These findings are novel in that potassium has primarily been associated with its BP lowering effects
[3,4,26,27]. Similar to our results, other data suggest that urinary sodium is not associated with AI as well
[Show abstract][Hide abstract] ABSTRACT: Increased potassium intake has been shown to lower blood pressure (BP) even in the presence of high sodium consumption however the role of dietary potassium on vascular function has received less attention. The aim of this study was to evaluate the relationship between habitual intake of sodium (Na) and potassium (K) and measures of arterial stiffness and wave reflection.
Thirty-six young healthy adults (21 M, 15 F; 24 +/- 0.6 yrs; systolic BP 117 +/- 2; diastolic BP 63 +/- 1 mmHg) recorded their dietary intake for 3 days and collected their urine for 24 hours on the 3rd day. Carotid-femoral pulse wave velocity (PWV) and the synthesis of a central aortic pressure waveform (by radial artery applanation tonometry and generalized transfer function) were performed. Aortic augmentation index (AI), an index of wave reflection, was calculated from the aortic pressure waveform.
Subjects consumed an average of 2244 kcals, 3763 mg Na, and 2876 mg of K. Average urinary K excretion was 67 +/- 5.3 mmol/24 hr, Na excretion was 157 +/- 11 mmol/24 hr and the average Na/K excretion ratio was 2.7 +/- 0.2. An inverse relationship between AI and K excretion was found (r = -0.323; p < 0.05). A positive relationship between AI and the Na/K excretion ratio was seen (r = 0.318; p < 0.05) while no relationship was noted with Na excretion alone (r = 0.071; p > 0.05). Reflection magnitude, the ratio of reflected and forward waves, was significantly associated with the Na/K excretion ratio (r = 0.365; p <0.05) but not Na or K alone. PWV did not correlate with Na or the Na/K excretion ratio (p > 0.05) but showed an inverse relationship with K excretion (r = -0.308; p < 0.05).
These data suggest that lower potassium intakes are associated with greater wave reflection and stiffer arteries in young healthy adults.
"The effect of sodium on blood pressure may, however, be modified by potassium intake or fluid intake, given their influence on blood pressure regulation and sodium homeostasis, which are both key functions of the kidney (Whelton et al, 1997; Rose and Post, 2001). That considered, potassium intake and fluid intake may individually influence RCC risk, or modify potential effects of sodium intake on RCC risk. "
[Show abstract][Hide abstract] ABSTRACT: Background:
As sodium, potassium and fluid intake are related to hypertension, an established risk factor for renal cell cancer (RCC), they may be independent risk factors for RCC.
The Netherlands Cohort Study (NLCS) with case-cohort design included 120 852 participants aged 55–69 years. At baseline, diet and lifestyle were assessed with questionnaires. After 17.3 years of follow-up, 485 RCC cases and 4438 subcohort members were available for analyses.
Sodium intake increased RCC risk (P-trend=0.03), whereas fluid and potassium intake did not. For high sodium and low fluid intake, the RCC risk additionally increased (P-interaction=0.02).
Sodium intake is a potential risk factor for RCC, particularly if fluid consumption is low.
British Journal of Cancer 12/2013; 110(3). DOI:10.1038/bjc.2013.771 · 4.84 Impact Factor
"Excessive salt consumption concerns many countries, so World Health Organization has promoted a less than 6 g daily intake to prevent stroke and heart disease
. Increased potassium intake has also been recommended for prevention and treatment of hypertension, especially in those who are unable to reduce their intake of sodium
[Show abstract][Hide abstract] ABSTRACT: Background
In kidney transplant (Kt) recipients , hypertension is a major risk for cardiovascular complications but also for graft failure. Blood pressure (BP) control is therefore mandatory. Office BP (OBP) remains frequently used for clinical decisions, however home BP (HBP) have brought a significant improvement in the BP control. Sodium is a modifiable risk factor, many studies accounted for a decrease of BP with a sodium restricted diet. Increased potassium intake has been also recommended in hypertension management. Using an agreement between office and home BP, the present study investigated the relations between the BP control in Kt recipients and their urinary excretion and dietary consumption of sodium and potassium.
The BP control defined by OBP <140/90 mmHg and HBP <135/85 mmHg was tested in 70 Kt recipients (mean age 56 ± 11.5 years; mean graft survival 7 ± 6.6 years) treated with antihypertensive medications. OBP and HBP were measured with a validated oscillometric device (Omron M6®). The 24-hour urinary sodium (Na+) and potassium (K+) excretions as well as dietary intakes were compared between controlled and uncontrolled (in office and at home) recipients. Non parametric Wilcoxon Mann–Whitney Test was used for between groups comparisons and Fisher's exact test for frequencies comparisons. Pearson correlation coefficients and paired t-test were used when sample size was >30.
Using an agreement between OBP and HBP, we identified controlled (21%) and uncontrolled recipients (49%). Major confounding effects susceptible to interfere with the BP regulation did not differ between groups, the amounts of sodium excretion were similar (154 ± 93 vs 162 ± 88 mmol/24 h) but uncontrolled patients excreted less potassium (68 ± 14 vs 54 ± 20 mmol/24 h; P = 0.029) and had significantly lower potassium intakes (3279 ± 753 vs 2208 ± 720 mg/24 h; P = 0.009), associated with a higher urinary Na+/K + ratio. Systolic HBP was inversely and significantly correlated to urinary potassium (r = −0.48; P = 0.002), a positive but non significant relation was observed with urinary sodium (r = 0,30;P = 0.074).
Half of the treated hypertensive Kt recipients remained uncontrolled in office and at home. Restoring a well-balanced sodium/potassium ratio intakes could be a non pharmacological opportunity to improve blood pressure control.
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