Dietary Potassium Supplementation Reduces Chronic Kidney Lesions Independent of Blood Pressure in Deoxycorticosterone-Acetate and High Sodium Chloride-Treated Mice.

We have previously shown that an excess of deoxycorticosterone acetate and high sodium chloride intake (DOCA/salt) in one-renin gene mice induces a high urinary Na/K ratio, hypokalemia, and cardiac and renal hypertrophy in the absence of hypertension. Dietary potassium supplementation prevents DOCA/salt-induced pathological processes. In the present study, we further study whether DOCA/salt-treated mice progressively develop chronic inflammation and fibrosis in the kidney and whether dietary potassium supplementation can reduce the DOCA/salt-induced renal pathological process. Results showed that (1) long-term DOCA/salt-treated one-renin gene mice developed severe kidney injuries including tubular/vascular hypertrophy, mesangial/interstitial/perivascular fibrosis, inflammation (lymphocyte's immigration), proteinuria, and high serum creatinine in the absence of hypertension; (2) there were over-expressed mRNAs of plasminogen activator inhibitor-1 (PAI-1), fibronectin, collagen type I and III, interferon-inducible protein-10 (IP-10), monocyte chemotactic protein-1 (MCP1), transforming growth factor-ß (TGF-ß), tumor necrosis factor-alpha (TNF-α), osteopontin, Nuclear factor kappa B (NF-κB)/P65, and intercellular adhesion molecule (ICAM)-1; and (3) dietary potassium supplementation normalized urinary Na/K ratio, hypokalemia, proteinuria, and serum creatinine, reduced renal hypertrophy, inflammations, and fibrosis, and down-regulated mRNA expression of fibronectin, Col-I and III, TGF-ß, TNF-α, osteopontin, and ICAM without changes in the blood pressure. The results provide new evidence that potassium and sodium may modulate proinflammatory and fibrotic genes, leading to chronic renal lesions independent of blood pressure.

Sodium-Reduced Meat and Poultry Products Contain a Significant Amount of Potassium from Food Additives.

BACKGROUND: Sodium-reduced packaged food products are increasingly available to consumers; however, it is not clear whether they are suitable for inclusion in a potassium-reduced diet. For individuals with impaired renal potassium excretion caused by chronic kidney disease and for those taking certain medications that interfere with the rennin-angiotensin aldosterone axis, the need to limit dietary potassium is important in view of the risk for development of hyperkalemia and fatal cardiac arrhythmias. OBJECTIVE: The primary objective of this study was to determine the impact of the reduction of sodium in packaged meat and poultry products (MPPs) on the content of potassium and phosphorus from food additives. DESIGN: This was a cross-sectional study comparing chemically analyzed MPPs (n=38, n=19 original, n=19 sodium-reduced), selected from the top three grocery chains in Canada, based on market share sales. All MPPs with a package label containing a reduced sodium content claim together with their non-sodium-reduced packaged MPP counterparts were selected for analysis. The protein, sodium, phosphorus, and potassium contents of sodium-reduced MPPs and the non-sodium-reduced (original) MPP counterparts were chemically analyzed according to the Association of Analytical Communities official methods 992.15 and 984.27 and compared by using a paired t test. The frequency of phosphorus and potassium additives appearing on the product labels' ingredient lists were compared between groups by using McNemar's test. RESULTS: Sodium-reduced MPPs (n=19) contained 44% more potassium (mg/100 g) than their non-sodium-reduced counterparts (n=19) (mean difference [95% CI): 184 [90-279]; P=0.001). The potassium content of sodium-reduced MPPs varied widely and ranged from 210 to 1,500 mg/100 g. Potassium-containing additives were found on the ingredient list in 63% of the sodium-reduced products and 26% of the non-sodium-reduced products (P=0.02). Sodium-reduced MPPs contained 38% less sodium (mg/100 g) than their non-sodium-reduced counterparts (mean difference [95% CI]: 486 [334-638]; P<0.001). The amounts of phosphorus and protein, as well as the frequency of phosphorus additives appearing on the product label ingredient list, did not significantly differ between the two groups. CONCLUSIONS: Potassium additives are frequently added to sodium-reduced MPPs in amounts that significantly contribute to the potassium load for patients with impaired renal handling of potassium caused by chronic kidney disease and certain medications. Patients requiring potassium restriction should be counseled to be cautious regarding the potassium content of sodium-reduced MPPs and encouraged to make food choices accordingly.

Short-Term High-Salt Diet Increases Corin Level to Regulate the Salt-Water Balance in Humans and Rodents.

BACKGROUND: Dietary sodium and potassium affect the fluctuation in blood pressure (BP) and renal function. Corin, with its enzymatic activity to convert pro-atrial natriuretic peptide (pro-ANP) to biologically active ANP, regulates BP, cardiac, and renal functions. We investigated whether corin expression responds to a high-salt (HS) diet to regulate salt and water balance. METHODS: Forty-two volunteers followed 3 sequential diets for 7 days each: a low-salt (LS) diet (3.0 g/day NaCl), a HS diet (18.0 g/day NaCl), followed by an HS diet with K+ supplementation (HS + K+) (18.0 g/day NaCl and 4.5 g/day KCl). RESULTS: Corin level was higher with the HS diet than the LS and HS + K+ diets and was positively correlated with systolic BP (SBP) and 24-hour urinary Na+ and microalbumin (U-mALB) excretion. In rodents, serum and renal levels of corin were transiently increased with the HS diet and were decreased if the HS diet was continued for up to 7 days. HS loading increased SBP, 24-hour urinary Na+, U-mALB excretion, and the expression of proprotein convertase subtilisin/kexin-6 (PCSK6), a corin activator. Knockdown of PCSK6 or corin in high salt-treated M1-cortical collecting duct (M1-CCD) cells increased the expression of aquaporin 2 (AQP2) and ß-epithelial Na+ channel (ß-ENaC). CONCLUSIONS: Short-term HS may induce the PCSK6-corin-ANP-AQP2/ß-ENaC pathway in the kidney. Enhanced serum corin level in humans and rodents is positively correlated with HS-induced SBP and 24-hour urinary Na+ and U-mALB excretion, which suggests that corin is involved in the salt-water balance in response to HS intake. CLINICAL TRIALS REGISTRATION: Public Trials Registry Number NCT02915315.

Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension.

Angiotensin II (AngII) hypertension increases distal tubule Na-Cl cotransporter (NCC) abundance and phosphorylation (NCCp), as well as epithelial Na(+) channel abundance and activating cleavage. Acutely raising plasma [K(+)] by infusion or ingestion provokes a rapid decrease in NCCp that drives a compensatory kaliuresis. The first aim tested whether acutely raising plasma [K(+)] with a single 3-hour 2% potassium meal would lower NCCp in Sprague-Dawley rats after 14 days of AngII (400 ng/kg per minute). The potassium-rich meal neither decreased NCCp nor increased K(+) excretion. AngII-infused rats exhibited lower plasma [K(+)] versus controls (3.6±0.2 versus 4.5±0.1 mmol/L; P<0.05), suggesting that AngII-mediated epithelial Na(+) channel activation provokes K(+) depletion. The second aim tested whether doubling dietary potassium intake from 1% (A1K) to 2% (A2K) would prevent K(+) depletion during AngII infusion and, thus, prevent NCC accumulation. A2K-fed rats exhibited normal plasma [K(+)] and 2-fold higher K(+) excretion and plasma [aldosterone] versus A1K. In A1K rats, NCC, NCCpS71, and NCCpT53 abundance increased 1.5- to 3-fold versus controls (P<0.05). The rise in NCC and NCCp abundance was prevented in the A2K rats, yet blood pressure did not significantly decrease. Epithelial Na(+) channel subunit abundance and cleavage increased 1.5- to 3-fold in both A1K and A2K; ROMK (renal outer medulla K(+) channel abundance) abundance was unaffected by AngII or dietary K(+) In summary, the accumulation and phosphorylation of NCC seen during chronic AngII infusion hypertension is likely secondary to potassium deficiency driven by epithelial Na(+) channel stimulation.

Potassium Intake, Bioavailability, Hypertension, and Glucose Control.

Potassium is an essential nutrient. It is the most abundant cation in intracellular fluid where it plays a key role in maintaining cell function. The gradient of potassium across the cell membrane determines cellular membrane potential, which is maintained in large part by the ubiquitous ion channel the sodium-potassium (Na+-K+) ATPase pump. Approximately 90% of potassium consumed (60-100 mEq) is lost in the urine, with the other 10% excreted in the stool, and a very small amount lost in sweat. Little is known about the bioavailability of potassium, especially from dietary sources. Less is understood on how bioavailability may affect health outcomes. Hypertension (HTN) is the leading cause of cardiovascular disease (CVD) and a major financial burden ($50.6 billion) to the US public health system, and has a significant impact on all-cause morbidity and mortality worldwide. The relationship between increased potassium supplementation and a decrease in HTN is relatively well understood, but the effect of increased potassium intake from dietary sources on blood pressure overall is less clear. In addition, treatment options for hypertensive individuals (e.g., thiazide diuretics) may further compound chronic disease risk via impairments in potassium utilization and glucose control. Understanding potassium bioavailability from various sources may help to reveal how specific compounds and tissues influence potassium movement, and further the understanding of its role in health.

The effect of dietary cation-anion difference concentration and cation source on milk production and feed efficiency in lactating dairy cows.

Feed costs currently account for 55% or more of the total cost of milk production in US dairy herds, and dairy producers are looking for strategies to improve feed efficiency [FE; 3.5% fat-corrected milk (FCM) per dry matter (DM) intake]. Increasing dietary cation-anion difference [DCAD; Na+K-Cl (mEq/kg of DM)] has been shown to increase milk production, FCM, and FE. However, the optimal DCAD concentration for maximal FE has yet to be determined. The objectives of this research were to test the effects of DCAD concentration and cation source on dairy FE. Sixty Holstein dairy cows (20 cows per experiment) were used in three 4×4 Latin square design experiments with 3-wk experimental periods. In experiments 1 and 2, we tested the effect of DCAD concentration: cows were fed a basal diet containing ~250 mEq/kg of DM DCAD that was supplemented with potassium carbonate at 0, 50, 100, and 150 mEq/kg of DM or 0, 125, 250, and 375 mEq/kg of DM in experiments 1 and 2, respectively. In experiment 3, we tested the effect of cation source: sodium sesquicarbonate replaced 0, 33, 67, and 100% of the supplemental potassium carbonate (150 mEq/kg of DM DCAD). The DCAD concentration had no effect on milk production, milk protein concentration, or milk protein yield in experiments 1 and 2. Dry matter intake was not affected by DCAD concentration in experiment 1 or by cation source in experiment 3. However, DMI increased linearly with increasing DCAD in experiment 2. We detected a linear increase in milk fat concentration and yield with increasing DCAD in experiments 1 and 2 and by substituting sodium sesquicarbonate for potassium carbonate in experiment 3. Increased milk fat concentration with increasing DCAD led to increases in 3.5% FCM in experiments 1 and 2. Maximal dairy FE was achieved at a DCAD concentration of 426 mEq/kg of DM in experiments 1 and 2 and by substituting Na for K in experiment 3. The results of these experiments suggest that both DCAD concentration and the cation source used to alter DCAD concentration have effects on milk fat content and yield and dairy FE.

Effect of dried California Mission figs on mineral status and food replacement.

OBJECTIVE: Figs are a rich source of several different minerals and fibres. We studied the effect of the consumption of dried California Mission figs on mineral and nutrient levels, as well as the effect of the addition of figs to a self-selected habitual diet on dietary patterns. DESIGN: A crossover randomized controlled trial study design in which participants with a mean of age of approximately 56 years were randomly assigned to eat either their usual diet for 5 weeks or to add dried California Mission figs (120 g/d) to their usual diet for 5 weeks, after which they crossed over to the other group for an additional 5 weeks. Six 24 h dietary recalls and four blood samples were obtained from each participant. SETTING: Loma Linda University School of Public Health, USA. SUBJECTS: A follow-up study using data collected from eighty-eight American males and females from September to December 2008. RESULTS: Diets reported in the 24 h dietary recall during the fig-supplemented diet period were significantly higher in Ca and K in the dietary and total phase (P value<0·05). Nevertheless, data on mineral levels in the body gathered by means of biochemical analyses from blood samples were nearly the same for both the figs-added and the participants' standard diet. The estimated displacement suggests that eating figs resulted in the elimination of 4% of desserts, 5% of vegetables, 10% of dairy products, 23% of grain products and 168% of beverages from other sources that participants would otherwise consume. CONCLUSIONS: Based on 24 h dietary recalls, the daily consumption of figs may increase the intake of several different minerals. However, mineral levels in blood samples were not altered significantly.

Application of photo-selective films to manipulate wavelength of transmitted radiation and photosynthate composition in red beet (Beta vulgaris var. conditiva Alef.).

BACKGROUND: Interest is increasing around both the use of plants as functional foods and the agronomic techniques which can increase nutrients and phytochemicals. Nevertheless, little research has focused on the effects of light on accumulation of active compounds in root storage organs. Red beet was treated with RED (red/far red ratio: 1.29; transmitted photosynthetically active radiation: 66.9%) and GREEN (red/far red ratio: 0.43; transmitted photosynthetically active radiation: 25.8%) photo-selective films and changes in nutrients and biomass accumulation were measured. RESULTS: Plants subjected to GREEN treatment had less dry weight accumulation both in storage roots (68%) and leaves (42%); moreover, soluble and structural carbohydrate concentration in roots was increased, as were the K, Mg and Zn concentrations (40.08, 2.95 and 0.023 mg g⁻¹ fresh weight, respectively). Conversely, GREEN lowered total phenolic concentration (0.33 vs. 0.47 mg g⁻¹ fresh weight) and antioxidant activity (0.65 vs. 0.94 µm Trolox equivalents g⁻¹ fresh weight) compared to CONTROL. Total pigment concentration was reduced by 20% and 48% with RED and GREEN treatments, respectively. CONCLUSION: Red beet showed a strong plasticity in its adaptation to light availability. Some macronutrients (fiber, sugars, minerals) can be concentrated in roots by modifying the amount and quality of the light, principally with GREEN photo-selective films.

Sodium and potassium and the pathogenesis of hypertension.

The evidence relating blood pressure to salt intake in humans originates from population studies and randomized clinical trials of interventions on dietary salt intake. Estimates from meta-analyses of trials in normotensive subjects generally are similar to estimates derived from prospective population studies (+1.7-mm Hg increase in systolic blood pressure per 100 mmol increment in 24-hour urinary sodium). This estimate, however, does not translate into an increased risk of incident hypertension in subjects consuming a high-salt diet. The meta-analyses of intervention trials have consistently shown that potassium supplementation is associated with lowering of blood pressure. However, prospective studies relating health outcomes to 24-hour urinary sodium and/or potassium excretion produced inconsistent results. Taken together, available evidence does not support the current recommendations of a generalized and indiscriminate reduction of salt intake at the population level, although the blood-pressure lowering effect of dietary sodium restriction might be of value in hypertensive patients. Potassium supplementation in hypertensive patients or healthy persons is not recommended by the current guidelines, but importance of adhering to healthy diet rich in vegetables and fruits is emphasized.

Effectiveness of potassium carbonate sesquihydrate to increase dietary cation-anion difference in early lactation cows.

The effect of additional dietary potassium in early lactation dairy cows was evaluated with the addition of potassium carbonate sesquihydrate, which increased dietary K from 1.3 to 2.1% of dry matter (DM) from wk 3 to 12 of lactation. Cows fed potassium carbonate sesquihydrate in the form of DCAD Plus (Church & Dwight Co. Inc., Princeton, NJ) had increased DM intake, milk fat percentage and yield, energy-corrected milk, and efficiency of milk production per unit of DM intake. Milk fat of cows fed higher dietary K had a lower concentration of trans fatty acids, suggesting a role for potassium carbonate sesquihydrate in the rumen in the biohydrogenation processes converting linoleic to stearic acid. Cows fed the diet with 2.1% K had greater apparent balance of K, and no effects were noted on the concentration of blood Mg or amount of fecal Mg. The data support the feeding of greater amounts of K in the early lactation cow.

Corn silage versus corn silage:alfalfa hay mixtures for dairy cows: effects of dietary potassium, calcium, and cation-anion difference.

Corn silage (CS) has replaced alfalfa hay (AH) and haylage as the major forage fed to lactating dairy cows, yet many dairy producers believe that inclusion of small amounts of alfalfa hay or haylage improves feed intake and milk production. Alfalfa contains greater concentrations of K and Ca than corn silage and has an inherently higher dietary cation-anion difference (DCAD). Supplemental dietary buffers such as NaHCO(3) and K(2)CO(3) increase DCAD and summaries of studies with these buffers showed improved performance in CS-based diets but not in AH-based diets. We speculated that improvements in performance with AH addition to CS-based diets could be due to differences in mineral and DCAD concentrations between the 2 forages. The objective of this experiment was to test the effects of forage (CS vs. AH) and mineral supplementation on production responses using 45 lactating Holstein cows during the first 20 wk postpartum. Dietary treatments included (1) 50:50 mixture of AH and CS as the forage (AHCS); (2) CS as the sole forage; and (3) CS fortified with mineral supplements (CaCO(3) and K(2)CO(3)) to match the Ca and K content of the AHCS diet (CS-DCAD). Feed intake and milk production were equivalent or greater for cows fed the CS and CS-DCAD diets compared with those fed the AHCS diet. Fat percentage was greater in cows fed the CS compared with the AHCS diet. Fat-corrected milk (FCM; 3.5%) tended to be greater in cows fed the CS and CS-DCAD diets compared with the AHCS diet. Feed efficiencies measured as FCM/dry matter intake were 1.76, 1.80, and 1.94 for the AHCS, CS, and CS-DCAD diets, respectively. The combined effects of reduced feed intake and increased FCM contributed to increased feed efficiency with the CS-DCAD diet, which contained 1.41% K compared with 1.18% K in the CS diet, and we speculate that this might be the result of added dietary K and DCAD effects on digestive efficiency. These results indicate no advantage to including AH in CS-based diets, but suggest that improving mineral supplementation in CS-based diets may increase feed efficiency.

Effects of anion supplementation to low-potassium prepartum diets on macromineral status and performance of periparturient dairy cows.

Data from multiparous Holstein cows (n = 43) were used to determine whether supplementation of anions to low-potassium (K) prepartum diets would improve periparturient energy and macromineral status and affect performance during the postpartum period. Beginning 21 d before expected parturition, cows were fed a control diet (1.29% K; +10 mEq/100 g; n = 21) or a low dietary cation-anion difference (DCAD) diet (1.29% K; -15 mEq/100 g; n = 22) with anions provided through a combination of sulfate from calcium sulfate dihydrate (0.40% S total ration) and chloride (1.17% Cl total ration) from SoyChlor 16-7 (West Central, Ralston, IA). All cows were fed the same postpartum diet from parturition through 63 d postpartum. Feeding anions decreased overall urine pH (8.17 vs. 6.70) during the prepartum period. Overall, peripartum concentrations of plasma Ca, P, and Mg were similar between treatments; however, concentrations of plasma Ca tended to be increased during the first 24 h postcalving in cows fed the low DCAD diet. Overall, concentrations of plasma P tended to be increased by feeding the anionic diet prepartum; this effect was more pronounced during the immediate peripartal period. Anionic supplementation did not affect incidence of clinical (<5 mg/dL) and subclinical (5 to 8 mg/dL) hypocalcemia, clinical hypophosphatemia (<2 mg/dL), or clinical (<1.1 mg/dL) and subclinical (1.1 to 1.8 mg/dL) hypomagnesemia. Nevertheless, subclinical hypophosphatemia (2 to 4 mg/dL) tended to be decreased at 16 h postcalving and was decreased at d 2 postpartum for cows fed the anionic diet prepartum. Anion supplementation decreased prepartum dry matter intake (15.6 vs. 14.4 kg/d), but did not affect postpartum dry matter intake (22.4 vs. 23.0 kg/d), milk yield (46.5 vs. 46.1 kg/d), or content and yield of milk fat and true protein. Plasma concentrations of energy-related metabolites (glucose, nonesterified fatty acids, beta-hydroxybutyrate) were similar for both groups during the prepartum and postpartum periods. Glucose rate of appearance was determined by continuous infusion of 6,6-dideuterated glucose in a subset of cows between 6 and 10 d prepartum (control, n = 12; low DCAD, n = 9) and 7 and 10 d postpartum (control, n = 9; low DCAD, n = 8) periods. Glucose rate of appearance was not affected by treatment during the prepartum or postpartum periods. Overall, anion supplementation of low K diets improved P status during the early postpartum period, but did not affect aspects of energy metabolism or periparturient performance.

Hypothetical hormonal mechanism by which potassium-rich diets benefit patients with rheumatoid arthritis.

Patients with rheumatoid arthritis (RA) have significantly lower salivary and serum potassium (K) concentration, reduced total body K, and lower dietary K intake than healthy subjects. There may also be a subtle impairment in the hypothalamic-pituitary-adrenal (HPA) axis in patients with RA with both a poor cortisol secretion response as well as a lower adrenocorticotropin hormone (ACTH) response in relation to involved inflammatory factors. Patients with RA also exhibit an impaired Na+, K+-ATPase (NKA) activity which might promote the pro-inflammatory cytokine secretion seen in RA. I will use these facts to support the mechanism I propose. There are no qualitative differences between the effects of endogenous cortisol and exogenously applied synthetic glucocorticoids (GCs), which are widely used to treat RA. All effects are transmitted via the same receptor. The GC, cortisol, plays a role in normal K homeostasis and the reverse is also seen with higher K intake leading to higher cortisol secretion and biosynthesis. Results of a recent clinical trial showed elevated serum cortisol followed K supplementation. I suggest that this is what alleviated RA symptoms. I would like to suggest a "Cortisol-K" theory as a mechanism for De Coti-Marsh's proposed "K theory" while not precluding the possibility of eventual proof of a cure, possibly from effects of K inside cells other than the adrenal glands.

Urinary kallikrein and blood pressure--gender-different response to potassium supplementation in SHR. Role of aldosterone.

AIMS: To test whether blood pressure is affected by potassium supplementation which modifies urinary kallikrein (UK) in SHR of either sex, and to elucidate the mechanisms involved. DESIGN: In SHR and WKY blood pressure, renal function and hormonal profile were studied after 1% oral potassium supplementation starting at 4 weeks of age and throughout until 12 weeks of age. Results were compared with those of untreated SHR and WKY of either sex. RESULTS: Systolic blood pressure (mm Hg) started to rise in SHR and was significantly different at 6-8 weeks of age: 153.5 +/- 7.9 versus 100 +/- 5.6 in female and 157 +/- 7.7 versus 98.4 +/- 6.8 in male rats (p < 0.01). Systolic blood pressure increased progressively in female and male rats reaching 164.5 +/- 4.8 and 204.5 +/- 7.6, respectively, at 12 weeks of age. At this time systolic blood pressure was higher in male than in female SHR (p < 0.01) and UK activity (UKa; nkat/day/100 g body weight) was slightly lower in male SHR. After 1% oral potassium supplementation administered from 4 to 12 weeks of age, a decrease in systolic blood pressure was seen in male SHR: 204.5 +/- 7.6 versus 173.5 +/- 7.9 (p < 0.05); and 164.5 +/- 4.8 versus 156.8 +/- 5.5 in female rats (NS) at 12 weeks of age, concomitant with an increase in UKa, particularly in male rats (29.35 +/- 1.92 versus 36.54 +/- 2.61, p < 0.05). As expected, plasma aldosterone (pg/ml), increased markedly after potassium treatment from 129 +/- 31.4 in untreated female and male SHR and WKY to 528 +/- 180.7 in SHR and 473 +/- 88.4 in WKY (p < 0.05 in both cases). After potassium supplementation, potassium excretion was significantly correlated with both aldosterone levels and UKa (p < 0.001 in both cases). No significantly concurrent changes in plasma renin activity were observed, but instead a significant decrease was seen in SHR (p < 0.01). The potassium blood pressure-lowering effect was blunted by aldosterone receptor antagonist treatment that also decreased UKa from 36.5 +/- 2.61 to 19.5 +/- 1.9, particularly in male SHR. No attempt was made in this experimental setting to block kallikrein or kinin receptors. CONCLUSIONS: UKa increases as a consequence of aldosterone stimulation by potassium load since an aldosterone receptor blockade abolishes UKa increment and blood pressure fall. These results further support the hypothesis that the kallikrein kinin system plays a role in blood pressure regulation and they also show a gender different response to potassium load in relation to UKa and blood pressure.

Dietary acid-base balance, bone resorption, and calcium excretion.

OBJECTIVE: Metabolic studies reveal that acidogenic diets increase bone resorption acutely. This study was conducted to examine associations between diet-induced changes in net acid excretion (NAE) and changes in serum parathyroid hormone (PTH), bone resorption, and calcium excretion over a longer period of 60 days. METHODS: Forty healthy older men and women were given 0.75 g/kg of protein as meat, 600 mg of calcium, and 400 IU of vitamin D3 daily and either cereal (acidogenic) or fruit and vegetable (alkalinogenic) foods as substitutes for some of the cereal in their usual diets. Blood and 24-hr urine measurements were made on days 14 (baseline), 44, and 74. RESULTS: In all subjects, change in renal NAE was correlated with changes in serum PTH (r = 0.358, P = 0.023), urinary N-telopeptide (NTX) (r = 0.367, P = 0.020), and urinary calcium excretion (rp = 0.381, P = 0.020, after adjustment for diet group, change in PTH, and change in sodium excretion). CONCLUSIONS: Diet changes that increase renal NAE are associated with increases in serum PTH, bone resorption, and calcium excretion over a 60-day period.

[The role of macro-elements in the human body]. / Az esszenciális makrofémionok szerepe az emberi szervezet muködésében.

The authors summarize the role of essential macro metal elements (Na, K, Ca, Mg) in human body: their homeostasis, absorption, transport, storage and excretion. Metabolism of macro-elements, daily requirements, cause of metal deficiencies and diseases caused by deficiencies are also discussed. Messenger and prooxidant effect of Ca2+-ions, indirect antioxidant effect of Mg2+-ions and the adjuvant application of magnesium are also reviewed.

Role of potassium in regulating blood flow and blood pressure.

Unlike sodium, potassium is vasoactive; for example, when infused into the arterial supply of a vascular bed, blood flow increases. The vasodilation results from hyperpolarization of the vascular smooth muscle cell subsequent to potassium stimulation by the ion of the electrogenic Na+-K+ pump and/or activating the inwardly rectifying Kir channels. In the case of skeletal muscle and brain, the increased flow sustains the augmented metabolic needs of the tissues. Potassium ions are also released by the endothelial cells in response to neurohumoral mediators and physical forces (such as shear stress) and contribute to the endothelium-dependent relaxations, being a component of endothelium-derived hyperpolarization factor-mediated responses. Dietary supplementation of potassium can lower blood pressure in normal and some hypertensive patients. Again, in contrast to NaCl restriction, the response to potassium supplementation is slow to appear, taking approximately 4 wk. Such supplementation reduces the need for antihypertensive medication. "Salt-sensitive" hypertension responds particularly well, perhaps, in part, because supplementation with potassium increases the urinary excretion of sodium chloride. Potassium supplementation may even reduce organ system complications (e.g., stroke).

Protective effects of dietary potassium chloride on hemodynamics of Dahl salt-sensitive rats in response to chronic administration of sodium chloride.

BACKGROUND: Dietary potassium supplementation decreases blood pressure and prevents strokes in humans, and prevents strokes and renal damage in Dahl salt-sensitive (DSS) rats. OBJECTIVE: To study the effects of various concentrations of dietary potassium chloride (KCl) on the hemodynamics of Dahl salt-resistant (DSR) and DSS rats receiving a 1% sodium chloride (NaCl) diet for 8 months, to determine whether there is an optimal dietary concentration of KCl that minimizes increases in blood pressure and causes least impairment of blood flow in the brain and kidneys. METHODS AND RESULTS: We found a biphasic effect on hemodynamic parameters as a function of dietary KCl in DSS rats of the Rapp strain fed 1% NaCl with increasing dietary KCl (0.7, 2.6, 4 and 8%). After 8 months receiving a diet containing 1% NaCl and 0.7% KCl, DSS rats had mean arterial pressures (MAP), plasma volumes, cardiac outputs and renal and cerebral vascular resistances that were significantly increased compared with those of DSR rats receiving the same diet. With a 2.6% KCl diet, all these parameters were significantly reduced compared with those in DSS rats fed the 0.7% KCl diet and were similar to those in DSR rats fed 2.6% KCl. Total peripheral resistance in DSR and DSS rats was similar on all diets. When KCl was increased to 4 and 8%, MAP, plasma volume, cardiac output and renal vascular resistance progressively increased in DSR and DSS rats, without changing total peripheral resistance. These changes paralleled increases in plasma aldosterone, which resulted from adrenocortical stimulation by the increasing dietary KCl; however, cerebral vascular resistance of DSR and DSS rats decreased significantly with a 4% KCl diet, despite increased aldosterone and sodium retention. Only DSS rats fed a 2.6% KCl diet had hemodynamics similar to those of DSR control rats fed the same diet, and hyperaldosteronism, sodium retention and increased plasma volume did not occur. CONCLUSION: 'Optimal' dietary KCl (2.6%) prevents hypertension and preserves cerebral and renal hemodynamics in DSS rats fed a diet containing 1% NaCl for 8 months, which causes hypertension when dietary KCl is limited or excessive.