Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Potassium, Dietary”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2002

Serum potassium level and dietary potassium intake as risk factors for stroke.

BACKGROUND: Numerous studies have found that low potassium intake and low serum potassium are associated with increased stroke mortality, but data regarding stroke incidence have been limited. Serum potassium levels, dietary potassium intake, and diuretic use in relation to risk for stroke in a prospectively studied cohort were investigated. METHODS: The study comprised 5,600 men and women older than 65 years who were free of stroke at enrollment. Baseline data included serum potassium level, dietary potassium intake, and diuretic use. Participants were followed for 4 to 8 years, and the incidence and types of strokes were recorded. Low serum potassium was defined as less than 4.1 mEq/L, and low potassium intake as less than 2.4 g/d. RESULTS: Among diuretic users, there was an increased risk for stroke associated with lower serum potassium (relative risk [RR]: 2.5, p < 0.0001). Among individuals not taking diuretics, there was an increased risk for stroke associated with low dietary potassium intake (RR: 1.5, p < 0.005). The small number of diuretic users with lower serum potassium and atrial fibrillation had a 10-fold greater risk for stroke compared with those with higher serum potassium and normal sinus rhythm. CONCLUSIONS: A lower serum potassium level in diuretic users, and low potassium intake in those not taking diuretics were associated with increased stroke incidence among older individuals. Lower serum potassium was associated with a particularly high risk for stroke in the small number of diuretic users with atrial fibrillation. Further study is required to determine if modification of these factors would prevent strokes.

Aged↗
PubMed2005

Low dietary potassium intakes and high dietary estimates of net endogenous acid production are associated with low bone mineral density in premenopausal women and increased markers of bone resorption in postmenopausal women.

BACKGROUND: The Western diet may be a risk factor for osteoporosis. Excess acid generated from high protein intakes increases calcium excretion and bone resorption. Fruit and vegetable intake could balance this excess acidity by providing alkaline salts of potassium. Algorithms based on dietary intakes of key nutrients can be used to approximate net endogenous acid production (NEAP) and to explore the association between dietary acidity and bone health. OBJECTIVE: We investigated the relation between dietary potassium and protein, NEAP (with an algorithm including the ratio of protein to potassium intake), and potential renal acid load (with an algorithm including dietary protein, phosphorous, potassium, magnesium, and calcium) and markers of bone health. DESIGN: Measurements of bone mineral density (BMD) (n = 3226) and urinary bone resorption markers (n = 2929) at the lumbar spine and femoral neck were performed in perimenopausal and early postmenopausal women aged 54.9 +/- 2.2 y (x +/- SD) in 1997-1999. BMD (g/cm(2)), free pyridinoline (fPYD), and free deoxypyridinoline (fDPD) were expressed relative to creatinine. Dietary intake was assessed with a food-frequency questionnaire. RESULTS: Comparison of the highest with the lowest quartile of potassium intake or the lowest with the highest NEAP showed a 6-8% increase in fPYD/creatinine and fDPD/creatinine. A difference of 8% in BMD was observed between the highest and lowest quartiles of potassium intake in the premenopausal group (n = 337). CONCLUSIONS: Dietary potassium, an indicator of NEAP and fruit and vegetable intake, may exert a modest influence on markers of bone health, which over a lifetime may contribute to a decreased risk of osteoporosis.

Acid-Base Equilibrium↗
PubMed1986

Relation between potassium excretion and proximal tubular fluid output in conscious unoperated rats adapted to different dietary potassium contents.

The effect of dietary potassium content on the proximal tubular fluid output (Vprox), and the relation between Vprox and potassium excretion was examined in conscious unoperated diabetes insipidus rats adapted to five dietary potassium contents in the range 25-400 mmol/kg. The lithium clearance (CLi) and the urine flow (V) were used as measures of Vprox, CLi being equal to and V being about one-third of Vprox. Increase of the dietary potassium content from 25 to 400 mmol/kg led only to a slight, barely statistically significant increase of Vprox. However, repeated measurements in the same rats on different days showed considerable intraindividual variation of Vprox and the potassium excretion. At each dietary potassium level except the lowest one the potassium excretion was linearly correlated to CLi (r = 0.60-0.92) and to V (r = 0.56-0.85). Errors in bladder emptying could not explain these correlations. The slopes of the regression lines increased with increasing dietary potassium content, and the regression lines all intercepted the CLi axis at approximately the same CLi value, i.e., on the average about 70 microliter/min./100 g body weight. The results indicate that an increase of the dietary potassium content leads to a slight increase of Vprox. Spontaneous intraindividual variation of Vprox is considerable and is associated with linearly related variation of the potassium excretion. The change of the potassium excretion for a given change of Vprox increases with the dietary potassium content.

Animals↗
PubMed1997

Relationship between turnover of cesium-137 and dietary potassium content in potassium-restricted mice.

The biological half-life of 137Cs and its organ distribution were investigated in mice fed various potassium-deficient diets. The biological half-life, which was 6.1 days in mice receiving the normal level of potassium, became longer as the dietary potassium content decreased, and 137Cs was hardly excreted from the body when dietary potassium content was restricted to 200 mg/kg or less. The muscle showed the highest concentration of 137Cs in both mice that had sufficient amounts of potassium and those that were potassium-deficient. Clearance of 137Cs from tissues was generally suppressed when mice were fed a potassium-deficient diet, but the relative distribution pattern of 137Cs was not affected by dietary potassium content. These results suggest that dietary potassium intake, which may vary with eating habits, affects the biological half-life of 137Cs in humans.

Animals↗
PubMed2000

Dietary potassium intake and stroke mortality.

BACKGROUND AND PURPOSE: An inverse relationship of dietary potassium to stroke mortality in a small community has been previously reported. To further assess this association in a larger sample, we examined data from the first National Health and Nutrition Examination Survey (NHANES I) Epidemiological Follow-up Study. METHODS: We analyzed baseline data during 1971-1975 and follow-up through 1992. Dietary potassium intake, determined by 24-hour dietary recall at baseline, was available for 9866 subjects. Stroke mortality was recorded through 1992 follow-up. RESULTS: Mean age and dietary potassium at baseline were 55 years and 2084 mg/d; blacks reported significantly lower potassium intake than whites (1606 versus 2178 mg/24 h). During an average of 16.7 years of follow-up, there were 304 stroke deaths. For men, stratified by tertile of dietary potassium intake, age-adjusted stroke mortality rates per 1000 person-years for the lowest dietary potassium group were significantly higher than for the highest intake group, for both whites (1.94 versus 1.17; relative risk, 1.66; 95% CI, 1.32 to 2.14) and blacks (5.08 versus 1.19; relative risk, 4.27; 95% CI, 1.88 to 9. 19). For women, there was no significant difference in stroke mortality between similar levels of potassium intake for either whites (1.61 versus 1.42; relative risk, 1.13; 95% CI, 0.84 to 1.66) or blacks (2.46 versus 3.04; relative risk, 0.80; 95% CI, 0.21 to 2. 01). After stratification by hypertensive status, stroke mortality rates were significantly different by tertile of dietary potassium only for hypertensive men. There was no stroke mortality difference by potassium intake among hypertensive women or nonhypertensive men and women. Multivariate analysis, in which we controlled for caloric intake and other baseline cardiovascular risk factors, revealed that only among black men and hypertensive men was lower dietary potassium intake a predictor of stroke mortality. CONCLUSIONS: The previous finding of an association of increasing dietary potassium intake with decreasing stroke mortality has been detected only among black men and hypertensive men in this study.

Adult↗
PubMed1985

The electrical basis for enhanced potassium secretion in rat distal colon during dietary potassium loading.

Previous studies in rat distal colon provide evidence for an active absorptive process for potassium under basal conditions, and for active potassium secretion during chronic dietary potassium loading. The present studies were performed with conventional and potassium-selective microelectrodes to determine the electrical basis for the increase in transcellular (active) potassium secretion observed during potassium loading. Compared to control tissues, potassium loading resulted in a 5-fold increase in transepithelial voltage (VT) and a 52% decrease in total resistance (RT) in the distal colon. The rise in VT was due to a decrease in apical membrane resistance and an increase in basolateral membrane voltage from -45 +/- 2 mV (cell interior negative) in control to -56 +/- 2 mV (p less than 0.001) in potassium loaded tissues. This difference in basolateral membrane voltage reflected in increase in intracellular potassium activity from 86 +/- 4 mM to 153 +/- 12 mM (P less than 0.001). In control tissues, the sequential mucosal addition of the sodium channel blocker amiloride (0.1 mM) and the potassium channel blocker tetraethylammonium chloride (TEA: 30 mM) produced no effect on the electrical measurements. However, in potassium loaded tissues, amiloride and TEA produced transepithelial changes consistent with inhibition of apical membrane conductances for sodium and potassium, respectively, reflected by increases in the resistance ratio, alpha (ratio of apical to basolateral membrane resistances). These data indicate that the decrease in apical membrane resistance during potassium loading was caused by an increase in apical membrane conductance for both potassium and sodium.

Amiloride↗
PubMed1985

Production and physiological responses of dairy cows to varying dietary potassium during heat stress.

Objectives were to study influences of heat stress and dietary potassium content on production and physiological responses of 8 Jersey and 10 Holstein cows blocked by breed and assigned randomly to no shade or shade environments. Each cow received a different dietary potassium treatment (.66, 1.08, and 1.64% of dry matter) in each of three 30-day periods. Rates of potassium loss from skin were almost five times greater for no shade as for shade cows during the hottest part of the day (1300 to 1500 h). Overall, cows with no shade ate 56% less during the daytime (0800 to 1600 h), 19% more during nighttime (1600 to 0800 h), and 13% less total feed than cows with shade. Interactions of environment and breed with dietary potassium treatment suggest differences in feed intake and milk yield responses to increasing dietary potassium content. Total daily feed intake and milk yield of cows with no shade responded in curvilinear fashion to increasing dietary potassium, whereas responses in shade were small. Largest responses in no shade were as dietary potassium increased from .66 to 1.08%. Milk yield of Holsteins increased with increasing dietary potassium, but yield of Jerseys did not. Combined effects of elevated potassium loss from skin and reduced potassium and dry matter intake during heat stress suggested that lactating dairy cows may benefit from supplemental potassium.

Analysis of Variance↗
PubMed1987

Increases in urinary kallikrein activity and prostanoid synthesis after dietary potassium supplementation.

1. To determine whether increasing dietary potassium alters kallikrein activity or prostaglandin synthesis, 77 women participated in a 3 week screening to assess their dietary potassium intake. Forty-four normotensive women whose dietary potassium was less than 60 mmol/day were allocated randomly to one of two groups who took either 80 mmol/day KCl (Slow-K, Ciba Geigy) or matching placebo for the first or second of two 4 week periods. 2. Significant increases in urinary kallikrein excretion (P less than 0.01), and urinary 6-keto-PGF1 alpha (P less than 0.01) were observed during potassium supplementation. These changes occurred without alterations in urine volume or sodium excretion. 3. It is suggested that potassium-induced changes in urinary 6-keto-PGF1 alpha may reflect increased renal and possibly vascular synthesis of prostacyclin. These increases may be mediated by increased plasma potassium stimulating kallikrein synthesis, leading to bradykinin-induced activation of phospholipase A2. Enhanced kallikrein/kinin and prostacyclin formation could contribute to the blood pressure lowering effect of potassium reported in hypertensive subjects.

6-Ketoprostaglandin F1 alpha↗
PubMed1978

Exercise performance and hemodynamics during dietary potassium depletion in dogs.

Dietary potassium depletion plus high sodium intake has been reported to elevate resting heart rate and cardiac output and to cause heart failure during exercise. We implanted aortic root electromagnetic flowmeters and aortic and pulmonary artery catheters in five splenectomized dogs condition-trained to run at 9 km/h on an 11% grade for 20 min. Postoperatively, the dogs ate a potassium-enriched diet until completion of control studies; then potassium was withdrawn. During 4 wk of depletion, skeletal muscle potassium fell from 380 +/- 22 to 311 +/- 8 meq/kg, and muscle sodium rose from 142 +/- 14 to 207 +/- 27 meq/kg (mean +/- SE). Cardiac output, aortic blood pressure, heart rate, acceleration of aortic blood flow at rest or during exercise, and the oxygen cost of exercise remained at control levels. Serum creatine phosphokinase at rest, an indicator of rhabdomyolysis, was never elevated. A 24% dietary depletion of muscle potassium in the dog did not change resting and exercise hemodynamics and exercise performance from control.

Animals↗
PubMed1995

Dietary potassium effects on lithium concentration and toxicity in hamsters.

Lithium can be toxic in rodents and human patients at concentrations within the therapeutic range for treatment of affective disorders. Diet containing supplemental potassium reduced lithium-induced weight loss in hamsters following daily injections of 3 mmol LiCl/kg for 7-10 days. Potassium supplementation also decreased lithium concentrations in peripheral tissues; but not in brain, after repeated lithium administration. Repeated lithium injection lowered the concentration of potassium in peripheral tissues, but tissue potassium was not restored by dietary potassium supplementation. Toxic effects of single injections of 1-10 mmol LiCl/kg were unaffected by dietary potassium. Lithium concentrations in plasma, brain, or peripheral tissues 6-hr after injection of 5 mmol LiCl/kg were also not altered by potassium diet. These data suggest that interactions between lithium and potassium diet differ in peripheral tissues compared to the central nervous system, and after acute versus chronic lithium administration.

Animals↗
PubMed2003

Nutritional and radiological impact of dietary potassium on the Pakistani population.

The nutritional status of dietary potassium and the radiological impact of its isotope (40)K were estimated for the Pakistani population. Potassium concentration was determined in dietary samples by atomic absorption spectrometry. An average potassium concentration was 4.54+/-0.89 mg/g, which leads to potassium dietary intake of 2.69+/-0.54 g/day and the radiological hazard due to (40)K activity was 79.94 Bq/day. The annual and lifetime effective doses calculated for the reference Pakistani man weighing 64 kg due to measured activity of (40)K were found to be 1.65 x 10(-4) Sv y(-1) and 8.27 x 10(-3) Sv, respectively. Measured data showed that the potassium concentration in the Pakistani diet is adequate and safe according to international standards.

Adult↗
PubMed1992

Effect of dietary potassium chloride in borderline hypertensive rats.

The borderline hypertensive rat is the first filial offspring of the spontaneously hypertensive rat and the Wistar-Kyoto rat. With increased dietary sodium chloride intake, the borderline hypertensive rat develops hypertension and exaggerated cardiovascular and renal responses to acute environmental stress, similar to those observed in the hypertensive spontaneously hypertensive rat parent. In other models of sodium chloride-sensitive hypertension with different genetic background (Dahl rat), dietary potassium chloride supplementation protects against the development of hypertension, increased sympathetic nervous system activity, and exaggerated responses to acute environmental stress. This investigation sought to determine whether the dietary sodium chloride-induced development of both the hypertension and the exaggerated responses to acute environmental stress could be reversed or prevented by increased dietary potassium chloride intake. Dietary potassium chloride intake was increased with a 1% potassium chloride drinking solution either after 12 wk of 8% sodium chloride intake (reversal) or concomitant with the onset of 12 wk of 8% sodium chloride intake (prevention). An increase in dietary potassium chloride intake did not reverse or prevent the development of either the hypertension or the exaggerated cardiovascular and renal responses to acute environmental stress in borderline hypertensive rats fed 8% sodium chloride. It is concluded that the difference in genetic background between borderline hypertensive rats and other models of sodium chloride-sensitive hypertension is an important determinant of the protective effect of dietary potassium chloride supplementation.

Animals↗
PubMed2000

Mechanism of antihypertensive effect of dietary potassium in experimental volume expanded hypertension in rats.

Dietary potassium supplementation lowers blood pressure (BP) and attenuates complications in hypertensive subjects, particularly those with the low renin volume expanded (LRVE) variety. We and others have shown that the plasma level of a digitalis like substance (DLS) is elevated in this type of hypertension. We therefore, examined the effect of increases in dietary potassium on the plasma level of endogenous DLS, myocardial and renal Na+, K+-ATPase (NKA) activities, BP, and renal excretory function in reduced renal mass (RRM)-salt hypertension in the rat, a classical model of LRVE hypertension. 70% RRM rats were divided in 4 groups, namely those consuming: 1) a sodium free and normal potassium (1.3% as KCl) diet (RRM-0 Na), 2) a normal sodium and normal potassium diet (RRM-NaK), 3) a normal sodium and high potassium (2 X normal) diet (RRM-Na2K), and 4) a normal sodium and 4 times normal potassium diet (RRM-Na4K). At the end of 4 weeks of dietary treatment, direct BP was recorded, plasma level of DLS determined by bioassay and with a radioimmunoassay for digoxin (DIF) and myocardial and renal NKA activities were measured. As expected, compared to RRM-0Na rats, RRM-NaK rats developed hypertension. BP increased significantly less in RRM-Na2K, whereas BP did not increase in RRM-Na4K rats. Hypertension in RRM-NaK rats was associated with an increase in plasma DLS and DIF and decrease in renal and myocardial NKA activities. DLS was increased (DIF was not changed) and myocardial NKA also decreased in rats consuming double potassium. However, quadrupling potassium in the diet (RRM-Na4K) normalized DLS and DIF and increased myocardial and renal NKA activities, compared to RRM-0Na rats. Also compared to RRM-0Na, water consumption, urinary volume excretion, sodium, and potassium increased in the other 3 groups, more so in RRM-Na4K rats. These data show that quadrupling the potassium in the diet prevents the BP increase in RRM rats and this is associated with diuresis/natriuresis and normalization of DLS, perhaps because the diuresis/natriuresis normalizes blood volume.

Animals↗
PubMed1997

Reduced dietary potassium reversibly enhances vasopressor response to stress in African Americans.

Acute vasopressor responses to stress are adrenergically mediated and hence potentially subject to differential modulation by dietary potassium and sodium. The greater vasopressor responsiveness in blacks compared with whites might then be consequent not only to a high dietary salt intake but also to a marginally reduced dietary potassium intake. Under controlled metabolic conditions, we compared acute vasopressor responses to cold and mental stress in black and white normotensive men during three successive dietary periods: (1) while dietary potassium was reduced (30 mmol K+/70 kg per day) and salt was restricted (10 to 14 days); (2) while salt was loaded (15 to 250 mmol Na+/70 kg per day) (7 days); and (3) while salt loading was continued and potassium was either supplemented (70 mmol K+/70 kg per day) (7 to 21 days) in 9 blacks and 6 whites or continued reduced (30 mmol K+/70 kg per day) (28 days) in 4 blacks (time controls). At the lower potassium intake, cold-induced increase in forearm vascular resistance in blacks was twice that in whites during both salt restriction and salt loading. Normalization of dietary potassium attenuated cold-induced increases in both forearm vascular resistance and systolic and diastolic blood pressures in blacks but only in systolic pressure in whites. In blacks but not in whites, normalization of dietary potassium attenuated mental stress-induced increases in systolic and diastolic pressures. In normotensive blacks but not whites, a marginally reduced dietary intake of potassium reversibly enhances adrenergically mediated vasopressor responsiveness to stress. That responsiveness so enhanced over time might contribute to the pathogenesis of hypertension in blacks.

Adult↗