Objective. —To assess the effects of supplementation with oral potassium on blood pressure in humans. Design. —Meta-analysis of randomized controlled trials. Data Sources. —English-language articles published before July 1995. Study Selection. —Thirty-three randomized controlled trials (2609 participants) in which potassium supplementation was the only difference between the intervention and control conditions. Data Extraction. —Using a standardized protocol, 2 of us independently abstracted information on sample size, duration, study design, potassium dose, participant characteristics, and treatment results. 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. Conclusions. —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.

https://jamanetwork.com/journals/JAMA/articlepdf/416446/jama_277_20_033.pdf

Effects of Oral Potassium on Blood Pressure: Meta-analysis of Randomized Controlled Clinical Trials

Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2004)

Sodium-to-Potassium Ratio and Blood Pressure, Hypertension, and Related Factors

Despite advances in the prevention and treatment of hypertension over the past decade, hypertension remains an important public health challenge. Recent efforts to reduce the prevalence of hypertension have focused on nonpharmacologic means, specifically diet. An increased intake of minerals such as potassium, magnesium, and calcium by dietary means has been shown in some but not all studies to reduce blood pressure in patients with hypertension. This review will discuss the roles of potassium, magnesium, and calcium in the prevention and treatment of essential hypertension with specific emphasis on clinical trial evidence, mechanism of action, and recommendations for dietary intake of these minerals. A high intake of these minerals through increased consumption of fruits and vegetables may improve blood pressure levels and reduce coronary heart disease and stroke.

/pdf/potassium-magnesium-and-calcium-their-role-in-both-the-cause-3wdxz9441k.pdf

Potassium, Magnesium, and Calcium: Their Role in Both the Cause and Treatment of Hypertension

A high-salt diet, which is known to contribute to the pathogenesis of hypertension, is also reportedly associated with insulin resistance. We investigated the effects of a high-salt diet on insulin sensitivity and insulin signaling in salt-sensitive (Dahl-S) and salt resistant (Dahl-R) strains of the Dahl rat. Evaluation of hyperinsulinemic-euglycemic clamp studies and glucose uptake into the isolated soleus muscle revealed that salt loading (8% NaCl) for 4 weeks induced hypertension and significant insulin resistance in Dahl-S rats, whereas no significant effects were observed in Dahl-R rats. Despite the presence of insulin resistance, insulin-induced tyrosine phosphorylation of the insulin receptor and insulin receptor substrates, activation of phosphatidylinositol 3-kinase, and phosphorylation of Akt were all enhanced in Dahl-S rats fed a high-salt diet. The mechanism underlying this form of insulin resistance thus differs from that previously associated with obesity and dexamethasone and is likely due to the impairment of one or more metabolic steps situated downstream of phosphatidylinositol 3-kinase and Akt activation. Interestingly, supplementation of potassium (8% KCl) ameliorated the changes in insulin sensitivity in Dahl-S rats fed a high-salt diet; this was associated with a slight but significant decrease in blood pressure. Evidence presented suggest that there is an interdependent relationship between insulin sensitivity and salt sensitivity of blood pressure in Dahl-S rats, and it is suggested that supplementing the diet with potassium may exert a protective effect against both hypertension and insulin resistance in salt-sensitive individuals.

High-salt diet enhances insulin signaling and induces insulin resistance in Dahl salt-sensitive rats.

To clarify the mechanism by which potassium (KCl) protects against the blood pressure rising action of sodium (NaCl), we studied the effects of KCl loading in patients with idiopathic hypertension who, after a period of NaCl restriction, partook of a high NaCl diet. Eleven patients who had taken the KCl supplement (96 mEq/day) during the high NaCl period showed lesser mean blood pressure (MAP) rise with changes in NaCl intake from 25 to 250 mEq/day than 12 patients who had not taken the KCl supplement (p less than 0.001). With a high NaCl diet, the KCl-supplemented patients retained less NaCl, gained less weight, and showed a lesser increase in plasma volume and cardiac output than the non-KCl-supplemented ones. Overall, the increase in blood pressure levels during the high Na diet correlated directly either with changes in plasma volume (p less than 0.05) or with changes in cardiac output (p less than 0.01). The results suggest that KCl may prevent a rise in blood pressure with NaCl loads in hypertensive patients by attenuating the increase in cardiac output, mainly as a result of the natriuresis. Furthermore, plasma norepinephrine was measured to estimate the sympathetic activity, since the sympathetic nervous system is known to control urinary NaCl excretion. From the low NaCl diet to Day 3 of the high NaCl diet, plasma norepinephrine was significantly (p less than 0.01) decreased in the KCl-supplemented patients, whereas it remained unchanged in the non-KCl-supplemented ones.(ABSTRACT TRUNCATED AT 250 WORDS)

T Fujita

Papers

Hemodynamic and endocrine changes associated with potassium supplementation in sodium-loaded hypertensives.