Relation of Cellular Potassium to Other Mineral Ions in Hypertension and Diabetes

Resnick, Lawrence M.; Barbagallo, Mario; Domínguez, Ligia J.; Veniero, Joseph M.; Nicholson, John; Gupta, Raj K.

doi:10.1161/01.hyp.38.3.709

Cited by 37 publications

(27 citation statements)

References 31 publications

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“…However, it was conducted on untreated hypertensive patients who are acknowledged to have a greater response to potassium (9,10) . In contrast to the results of other authors (22,32) we did not find any correlation between RBC-K and baseline BP levels nor did we observe an effect of supplementation on RBC-K. An explanation for the present result may partially arise from the fact that the sample of participants was relatively small and composed largely of young healthy normotensive subjects.…”

Section: Discussioncontrasting

confidence: 99%

The effect of a dietary supplement of potassium chloride or potassium citrate on blood pressure in predominantly normotensive volunteers

Braschi

Naismith

2008

Br J Nutr

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Blood pressure (BP) shows a continuous relationship with the risk of CVD. There is substantial evidence that dietary potassium exerts an antipressor effect. Most clinical trials have used KCl. However, the chloride ion may have a pressor effect and in foods potassium is associated with organic anions. In a double-blind randomized placebo-controlled trial we explored the effect on BP of two salts of potassium, KCl and potassium citrate (K-cit), in predominantly young healthy normotensive volunteers. The primary outcome was the change in mean arterial pressure as measured in a clinic setting. After 6 weeks of supplementation, compared with the placebo group (n 31), 30 mmol K-cit/d (n 28) changed mean arterial pressure by 25·22 mmHg (95 % CI 2 8·85, 24·53) which did not differ significantly from that induced by KCl (n 26), 2 4·70 mmHg (2 6·56, 22·84). The changes in systolic and diastolic BP were 26·69 (95 % CI 2 8·85, 24·43) and 2 4·26 (95 % CI 26·31, 2 2·21) mmHg with K-cit and 25·24 (95 % CI 2 7·43, 23·06) and 24·30 (95 % CI 26·39, 22·20) mmHg with KCl, and did not differ significantly between the two treatments. Changes in BP were not related to baseline urinary electrolytes. A greater treatment-related effect was observed in those with higher systolic BP. Increasing dietary potassium could therefore have a significant impact on the progressive rise in BP in the entire population.

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Section: Discussioncontrasting

confidence: 99%

The effect of a dietary supplement of potassium chloride or potassium citrate on blood pressure in predominantly normotensive volunteers

Braschi

Naismith

2008

Br J Nutr

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“…14 Recently, it has been shown that RBC Ki measured by nuclear magnetic resonance is significantly decreased in hypertensives and that treatment of hypertension partially restores RBC Ki levels. 15 This observation confirms our previous report showing that hypertensive patients with low RBC Ki who received antihypertensive therapy and K + sparing drugs had a significant improvement in BP, RBC Ki , and fasting glucose levels. 16 The effect of K + depletion on insulin sensitivity 17 and on insulinstimulated cell K + uptake 18 could explain why hypertensives have decreased RBC Ki and increased glucose levels compared to hypertensives.…”

Section: Discussionsupporting

confidence: 91%

Red blood cell K+ could be a marker of K+ changes in other cells involved in blood pressure regulation

Delgado

Delgado-Almeida

2003

J Hum Hypertens

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The aim of this study is to determine whether red blood cell K + content (RBC Ki ) is associated with blood pressure levels and, if so, could RBC Ki be a marker of potassium changes in other cells involved in blood pressure regulation. The study was performed on 50 untreated hypertensives, 32 of their offspring and 50 age-and sex-matched controls. Systolic (SBP) and diastolic (DBP) blood pressures, height, weight, plasma, urine and red blood cell electrolytes were measured in all subjects. RBC Ki was significantly lower in hypertensives than in offspring of hypertensives and normotensive controls. Offspring of hypertensives had significantly lower RBC Ki than normotensive controls. Plasma K + was significantly lower both in hypertensives and offspring of hypertensives when compared to normotensive controls. A significant negative correlation was found in hypertensives between RBC Ki and DBP (r ¼ À0.27, P ¼ 0.04) and in offspring of hypertensives between RBC Ki and DBP (r ¼ À0.43, P ¼ 0.02). A significant correlation was found in hypertensives between RBC Ki and plasma K + (r ¼ 0.3, P ¼ 0.02). A positive correlation with borderline significance was found in hypertensives between RBC Ki and ionized Ca 2+ (r ¼ 0.2, P ¼ 0.1). In conclusion, our results support the hypothesis that RBC Ki is associated with blood pressure levels and that the measurement of RBC Ki levels may represent a biochemical marker for K + changes in other cells involved in blood pressure regulation. Further studies are necessary to explain the exact mechanisms of reduced RBC Ki levels in hypertensive patients and their offspring.

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“…With 30 mmol/day potassium in the diet, salt loading slightly increased BP only in Blacks, but 70 mmol/day potassium load attenuated, and 120 mmol/day, completely abolished, salt sensitivity in both Blacks and Whites [116]. This is especially important since cellular potassium was lower in hypertensives, and this was further exacerbated by saline infusion [117]. In Finland, among high salt intake hypertensives, there was no difference in potassium excretion or sodium/potassium ratio, but half the patients were on anti-hypertensive medication, which could have affected the results [118].…”

Section: Potassium the Forgotten Cationmentioning

confidence: 99%

Salt and hypertension: a phylogenetic perspective

Lev-Ran

Porta

2005

Diabetes Metab. Res. Rev.

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Our hunter-gatherer ancestors appeared to survive on little salt. When today's rural dwellers move to urban environments, they increase their salt intake and the salt-sensitive among them become prone to age-related increase in blood pressure and hypertension. This paper reviews our knowledge of the mechanisms of salt disposal and plasma volume regulation, salt consumption in human evolution, salt intake and prevalence of hypertension, and the results of interventions aimed at modulating both. Finally, it discusses current hypotheses on the mechanisms of selective pressure that may have favored the emergence of a salt-sensitive, hypertensive genotype. Similar to 'thrifty' genes, which supported energy savers in times of scarcity, but may now be causing obesity and type 2 diabetes, 'thirsty' genes, by acting on salt and water retention, might have helped individuals survive the challenge of volume-depleting illnesses, especially when combined with stress-inducing situations, but may now cause high BP and related damage in the post-reproductive age.

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Relation of Cellular Potassium to Other Mineral Ions in Hypertension and Diabetes

Cited by 37 publications

References 31 publications

The effect of a dietary supplement of potassium chloride or potassium citrate on blood pressure in predominantly normotensive volunteers

The effect of a dietary supplement of potassium chloride or potassium citrate on blood pressure in predominantly normotensive volunteers

Red blood cell K+ could be a marker of K+ changes in other cells involved in blood pressure regulation

Salt and hypertension: a phylogenetic perspective

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