Effect of Increased Potassium Intake on Adrenal Cortical and Cardiovascular Responses to Angiotensin II: A Randomized Crossover Study.

Background Increased potassium intake lowers blood pressure in patients with hypertension, but increased potassium intake also elevates plasma concentrations of the blood pressure-raising hormone aldosterone. Besides its well-described renal effects, aldosterone is also believed to have vascular effects, acting through mineralocorticoid receptors present in endothelial and vascular smooth muscle cells, although mineralocorticoid receptors-independent actions are also thought to be involved. Methods and Results To gain further insight into the effect of increased potassium intake and potassium-stimulated hyperaldosteronism on the human cardiovascular system, we conducted a randomized placebo-controlled double-blind crossover study in 25 healthy normotensive men, where 4 weeks treatment with a potassium supplement (90 mmol/day) was compared with 4 weeks on placebo. At the end of each treatment period, we measured potassium and aldosterone in plasma and performed an angiotensin II (AngII) infusion experiment, during which we assessed the aldosterone response in plasma. Hemodynamics were also monitored during the AngII infusion using ECG, impedance cardiography, finger plethysmography (blood pressure-monitoring), and Doppler ultrasound. The study showed that higher potassium intake increased plasma potassium (mean±SD, 4.3±0.2 versus 4.0±0.2 mmol/L; P=0.0002) and aldosterone (median [interquartile range], 440 [336-521] versus 237 [173-386] pmol/L; P<0.0001), and based on a linear mixed model for repeated measurements, increased potassium intake potentiated AngII-stimulated aldosterone secretion (P=0.0020). In contrast, the hemodynamic responses (blood pressure, total peripheral resistance, cardiac output, and renal artery blood flow) to AngII were similar after potassium and placebo. Conclusions Increased potassium intake potentiates AngII-stimulated aldosterone secretion without affecting systemic cardiovascular hemodynamics in healthy normotensive men. Registration EudraCT Number: 2013-004460-66; URL: https://www.ClinicalTrials.gov; Unique identifier: NCT02380157.

Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake.

BACKGROUND: The basolateral potassium channel in the distal convoluted tubule (DCT), comprising the inwardly rectifying potassium channel Kir4.1/Kir5.1 heterotetramer, plays a key role in mediating the effect of dietary potassium intake on the thiazide-sensitive NaCl cotransporter (NCC). The role of Kir5.1 (encoded by Kcnj16) in mediating effects of dietary potassium intake on the NCC and renal potassium excretion is unknown. METHODS: We used electrophysiology, renal clearance, and immunoblotting to study Kir4.1 in the DCT and NCC in Kir5.1 knockout (Kcnj16-/- ) and wild-type (Kcnj16+/+ ) mice fed with normal, high, or low potassium diets. RESULTS: We detected a 40-pS and 20-pS potassium channel in the basolateral membrane of the DCT in wild-type and knockout mice, respectively. Compared with wild-type, Kcnj16-/- mice fed a normal potassium diet had higher basolateral potassium conductance, a more negative DCT membrane potential, higher expression of phosphorylated NCC (pNCC) and total NCC (tNCC), and augmented thiazide-induced natriuresis. Neither high- nor low-potassium diets affected the basolateral DCT's potassium conductance and membrane potential in Kcnj16-/- mice. Although high potassium reduced and low potassium increased the expression of pNCC and tNCC in wild-type mice, these effects were absent in Kcnj16-/- mice. High potassium intake inhibited and low intake augmented thiazide-induced natriuresis in wild-type but not in Kcnj16-/- mice. Compared with wild-type, Kcnj16-/- mice with normal potassium intake had slightly lower plasma potassium but were more hyperkalemic with prolonged high potassium intake and more hypokalemic during potassium restriction. CONCLUSIONS: Kir5.1 is essential for dietary potassium's effect on NCC and for maintaining potassium homeostasis.

Bioavailability of potassium from potatoes and potassium gluconate: a randomized dose response trial.

BACKGROUND: The bioavailability of potassium should be considered in setting requirements, but to our knowledge, the bioavailability from individual foods has not been determined. Potatoes provide 19-20% of potassium in the American diet. OBJECTIVE: We compared the bioavailability and dose response of potassium from nonfried white potatoes with skin [targeted at 20, 40, and 60 milliequivalents (mEq) K] and French fries (40 mEq K) with potassium gluconate at the same doses when added to a basal diet that contained ∼60 mEq K. DESIGN: Thirty-five healthy, normotensive men and women with a mean ± SD age of 29.7 ± 11.2 y and body mass index (in kg/m(2)) of 24.3 ± 4.4 were enrolled in a single-blind, crossover, randomized controlled trial. Participants were partially randomly assigned to the order of testing for nine 5-d interventions of additional potassium as follows: 0 (control; repeated at phases 1 and 5), 20, 40, and 60 mEq K/d consumed as a potassium gluconate supplement or as unfried potato or 40 mEq K from French fries completed at phase 9. The bioavailability of potassium was determined from the area under the curve (AUC) of serial blood draws and cumulative urinary excretion during a 24-h period and from a kinetic analysis. The effects of the potassium source and dose on the change in blood pressure and augmentation index (AIx) were determined. RESULTS: The serum potassium AUC increased with the dose (P < 0.0001) and did not differ because of the source (P = 0.53). Cumulative 24-h urinary potassium also increased with the dose (P < 0.0001) and was greater with the potato than with the supplement (P < 0.0001). The kinetic analysis showed the absorption efficiency was high across all interventions (>94% ± 12%). There were no significant differences in the change in blood pressure or AIx with the treatment source or dose. CONCLUSIONS: The bioavailability of potassium is as high from potatoes as from potassium gluconate supplements. Future studies that measure the effect of dietary potassium on blood pressure will need to evaluate the effect of various dietary sources on potassium retention and in both normal and hypertensive populations. This trial was registered at clinicaltrials.gov as NCT01881295.

Traditional and novel dietary interventions for preventing progression of chronic kidney disease.

Treatment of chronic kidney disease (CKD) and its complications remain largely unresolved. Currently used treatments include blood pressure control and the use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), which can slow down the progression of CKD but are unable to halt or reverse it. Dietary protein restriction represents an additional therapeutic measure used to slow the progression of CKD. The putative mechanisms of action responsible for its therapeutic effects include beneficial hemodynamic effects and the limitation of absorbable protein breakdown products that could lead to the accumulation of uremic waste and consequent various deleterious effects. The practical implementation of protein restriction through dietary intervention has been hindered on multiple levels, including patient nonadherence, lack of health care resources, and concerns related to adverse effects associated with the development of protein-energy wasting (PEW). As a result, alternative interventions have been designed to address some or all of these shortcomings and concerns. One such intervention is the administration of medications that prevent the absorption of protein catabolic products from the gut. This article reviews the various interventions using such a strategy to prevent or slow the progression of CKD, with special focus on recent advances in this field.

Serum and dietary potassium and risk of incident type 2 diabetes mellitus: The Atherosclerosis Risk in Communities (ARIC) study.

BACKGROUND: Serum potassium levels affect insulin secretion by pancreatic ß-cells, and hypokalemia associated with diuretic use has been associated with dysglycemia. We hypothesized that adults with lower serum potassium levels and lower dietary potassium intake are at higher risk for incident diabetes mellitus (DM), independent of diuretic use. METHODS: We analyzed data from 12 209 participants from the Atherosclerosis Risk in Communities (ARIC) Study, an ongoing prospective cohort study, beginning in 1986, with 9 years of in-person follow-up and 17 years of telephone follow-up. Using multivariate Cox proportional hazard models, we estimated the hazard ratio (HR) of incident DM associated with baseline serum potassium levels. RESULTS: During 9 years of in-person follow-up, 1475 participants developed incident DM. In multivariate analyses, we found an inverse association between serum potassium and risk of incident DM. Compared with those with a high-normal serum potassium level (5.0-5.5 mEq/L), adults with serum potassium levels lower than 4.0 mEq/L, 4.0 to lower than 4.5 mEq/L, and 4.5 to lower than 5.0 mEq/L had an adjusted HR (95% confidence interval [CI]) of incident DM of 1.64 (95% CI, 1.29-2.08), 1.64 (95% CI, 1.34-2.01), and 1.39 (95% CI, 1.14-1.71), respectively. An increased risk persisted during an additional 8 years of telephone follow-up based on self-report with HRs of 1.2 to 1.3 for those with a serum potassium level lower than 5.0 mEq/L. Dietary potassium intake was significantly associated with risk of incident DM in unadjusted models but not in multivariate models. CONCLUSIONS: Serum potassium level is an independent predictor of incident DM in this cohort. Further study is needed to determine if modification of serum potassium could reduce the subsequent risk of DM.

Precaecal and postileal metabolism of P, Ca and N in pigs as affected by different carbohydrate sources fed at low level of P intake.

Three different carbohydrate sources (cellulose on wood basis, maize starch and apple pectin) in combination with a low phosphorus (P) basal diet were fed to eight pigs fitted with single ileum-T-cannulas in a balance trial. The effects on net disappearance of dry matter, N, P and Ca as well as phytate (IP6) degradation in the intestine were studied. A basal diet and three diets supplemented with 25% of one carbohydrate source were applied in three experimental periods following an incomplete Latin Square design. Animals were housed individually in balance crates. After 15 days of adaptation to the diets, five days of total excreta collection were followed by two days of spot sampling of ileal digesta. The results showed a significantly decreasing effect of cellulose on the precaecal, postileal and total tract digestibility of DM, N and P. Starch reduced precaecal IP6 degradation and P digestibility. The addition of pectin negatively affected the precaecal digestibility of DM, N and Ca as well as the total tract digestibility of P and Ca. Postileally, cellulose and pectin caused a net secretion while starch induced a net absorption of P.

Kir4.1/Kir5.1 channel forms the major K+ channel in the basolateral membrane of mouse renal collecting duct principal cells.

K(+) channels in the basolateral membrane of mouse cortical collecting duct (CCD) principal cells were identified with patch-clamp technique, real-time PCR, and immunohistochemistry. In cell-attached membrane patches, three K(+) channels with conductances of approximately 75, 40, and 20 pS were observed, but the K(+) channel with the intermediate conductance (40 pS) predominated. In inside-out membrane patches exposed to an Mg(2+)-free medium, the current-voltage relationship of the intermediate-conductance channel was linear with a conductance of 38 pS. Addition of 1.3 mM internal Mg(2+) had no influence on the inward conductance (G(in) = 35 pS) but reduced outward conductance (G(out)) to 13 pS, yielding a G(in)/G(out) of 3.2. The polycation spermine (6 x 10(-7) M) reduced its activity on inside-out membrane patches by 50% at a clamp potential of 60 mV. Channel activity was also dependent on intracellular pH (pH(i)): a sigmoid relationship between pH(i) and channel normalized current (NP(o)) was observed with a pK of 7.24 and a Hill coefficient of 1.7. By real-time PCR on CCD extracts, inwardly rectifying K(+) (Kir)4.1 and Kir5.1, but not Kir4.2, mRNAs were detected. Kir4.1 and Kir5.1 proteins cellularly colocalized with aquaporin 2 (AQP2), a specific marker of CCD principal cells, while AQP2-negative cells (i.e., intercalated cells) showed no staining. Dietary K(+) had no influence on the properties of the intermediate-conductance channel, but a Na(+)-depleted diet increased its open probability by approximately 25%. We conclude that the Kir4.1/Kir5.1 channel is a major component of the K(+) conductance in the basolateral membrane of mouse CCD principal cells.

Renal and gastrointestinal potassium excretion in humans: new insight based on new data and review and analysis of published studies.

OBJECTIVES: Little is known about the relationship between the renal and gastrointestinal excretion of potassium in humans. This information is important in light of strong associations of potassium intake with hypertension and occlusive stroke. METHODS: We determined the relationship between fecal and urinary excretion of potassium under both fixed and variable potassium intakes using our unpublished archival data and published data of others. Twenty-five subjects were evaluated. RESULTS: On a fixed, low oral potassium intake (61.2 +/- 4.7 mmol/day; mean +/- SD), there was an inverse relationship between fecal and urinary potassium excretion (r = -0.66, p = 0.040). In studies in which potassium intake varied between 61-135 mmol/day, fecal and urinary potassium excretions were positively correlated (r = 0.58, p = 0.024). Considerable within-and-between-subject variation was observed in the relationship between fecal and urinary potassium excretion. CONCLUSIONS: Inter-individual variation in fecal potassium excretion may arise from both variation in dietary potassium intake and intrinsic individual differences in the renal versus gastrointestinal handling of potassium.

[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.

Protective effects of high dietary potassium: nutritional and metabolic aspects.

Potassium (K+) requirements have been largely overlooked because severe deficiencies are uncommon due to the ubiquity of this element in foods. However, a transition toward modern ("Westernized") diets has led to a substantial decline of K+ intake compared with traditional food habits, and a large fraction of the population might now have suboptimal K+ intake. A high K+ intake was demonstrated to have protective effects against several pathologic states affecting the cardiovascular system, kidneys, and bones. Additionally, fruits and vegetables contain K/organic anion salts (malate, citrate), which exert alkalinizing effects, through KHCO(3)(-) generation, which serves to neutralize fixed acidity in urine. Low-grade metabolic acidosis, when not properly controlled, may exacerbate various catabolic processes (bone Ca++ mobilization, proteolysis), especially in the elderly. Fruits and vegetables are therefore receiving great attention in a strategy to increase the nutritional value of meals while reducing energy density and intake. The need to ensure a 2.5- to 3.5-g daily K+ supply from fruits and vegetables represents a strong rationale for the "5-10 servings per day" recommendations.

Effect of spironolactone on K(+) homeostasis and ENaC expression in lymphocytes from chronic hemodialysis patients.

BACKGROUND: Cardiac disease is the major cause of death in hemodialysis patients (HD). It is now clear that aldosterone has deleterious effects in the cardiovascular system. In the present study, we evaluated the effects of an aldosterone-antagonist, spironolactone, on the extrarenal regulation of potassium in HD patients. Furthermore, to validate the effectiveness of the spironolactone dose-design, we measured the expression of Na(+)-channel (ENaC alpha subunit) in peripheral blood mononuclear cells (PBMC), before and after a two-week course of spironolactone. METHODS: The study design included a two-week baseline period, followed by spironolactone treatment (50 mg three times weekly for 15 days), and by a two-week washout period and then a two-week placebo period. An oral K(+) load (0.3 mEq/K(+) kg body weight plus carbohydrates) was administered at the end of each period, and time-course of plasma potassium was evaluated. ENaC expression in PBMC was assessed before and after spironolactone. RESULTS: The maximal increase in plasma potassium after the K(+) carbohydrate load was: control 5.33 +/- 0.88 mEq K(+)/L; spironolactone 5.23 +/- 0.68 mEq K(+)/L; placebo 5.38 +/- 0.61 mEq K(+)/L (N= 9). No patients developed hyperkalemia during the spironolactone treatment period. ENaC expression was significantly higher in all six HD patients studied, compared to control subjects (P < 0.05). Treatment with spironolactone in HD patients reduced alpha subunit mRNA expression to values similar to those of normal subjects. CONCLUSION: Spironolactone may be considered for the treatment of selected chronic HD patients. The effect of the drug on a known target of aldosterone, the ENaC, demonstrates the effectiveness of the drug to block aldosterone effects in nonepithelial tissues.

Dietary potential renal acid load and renal net acid excretion in healthy, free-living children and adolescents.

BACKGROUND: There is increasing evidence that acid-base status has a significant effect on high-intensity physical performance, urolithiasis, and calcium metabolism. Experimental studies in adults showed that renal net acid excretion (NAE) can be reliably estimated from the composition of diets. OBJECTIVE: We investigated whether a reasonable estimation of NAE is also possible from the dietary records of free-living children and adolescents. DESIGN: Healthy children (aged 8 y; n = 165) and adolescents (aged 16-18 y; n = 73) each collected a 24-h urine sample and completed a weighed diet record on the same day. Urinary NAE was analyzed (NAE(an)) and estimated (NAE(es)). Potential renal acid load (PRAL), the diet-based component of NAE(es), corrects for intestinal absorption of ingested minerals and sulfur-containing protein. A urinary excretion rate of organic acids (OAs) proportional to body surface area was assumed for the complete estimate (NAE(es) = PRAL + OA(es)). RESULTS: Significant (P < 0.001) correlations between NAE(es) and NAE(an) were seen in the children (r = 0.43) and the adolescents (r = 0.51). A simplified estimate based on only 4 components of dietary PRAL (protein, phosphorus, potassium, and magnesium) yielded almost identical associations. Mean simplified NAE(es) (32.6 +/- 13.9 and 58.4 +/- 22.0 mEq/d in the children and the adolescents, respectively) agreed reasonably with NAE(an) (32.4 +/- 15.5 and 52.8 +/- 24.3 mEq/d, respectively). CONCLUSIONS: Predicting NAE from dietary intakes, food tables, and anthropometric data is also applicable during growth and yields appropriate estimates even when self-selected diets are consumed. The PRAL estimate based on only 4 nutrients may allow relatively simple assessment of the acidity of foods and diets.

Active K+ secretion through multiple KCa-type channels and regulation by IKCa channels in rat proximal colon.

Colonic K+ secretion stimulated by cholinergic agents requires activation of muscarinic receptors and the release of intracellular Ca2+. However, the precise mechanisms by which this rise in Ca2+ leads to K+ efflux across the apical membrane are poorly understood. In the present study, Northern blot analysis of rat proximal colon revealed the presence of transcripts encoding rSK2 [small conductance (SK)], rSK4 [intermediate conductance (IK)], and rSlo [large conductance (BK)] Ca2+-activated K+ channels. In dietary K+-depleted animals, only rSK4 mRNA was reduced in the colon. On the basis of this observation, a cDNA encoding the K+ channel rSK4 was cloned from a rat colonic cDNA library. Transfection of this cDNA into Chinese hamster ovary (CHO) cells led to the expression of Ca2+-activated K+ channels that were blocked by the IK channel inhibitor clotrimazole (CLT). Confocal immunofluorescence confirmed the presence of IK channels in proximal colonic crypts, and Western blotting demonstrated that IK protein sorted to both the apical and basolateral surfaces of colonic epithelia. In addition, transcellular active K+ secretion was studied on epithelial strips of rat proximal colon using unidirectional 86Rb+ fluxes. The addition of thapsigargin or carbachol to the serosal surface enhanced net 86Rb+ secretion. The mucosal addition of CLT completely inhibited carbachol-induced net 86Rb+ secretion. In contrast, only partial inhibition was observed with the BK and SK channel inhibitors, iberiotoxin and apamin, respectively. Finally, in parallel with the reduction in SK4 message observed in animals deprived of dietary K+, carbachol-induced 86Rb+ secretion was abolished in dietary K+-depleted animals. These results suggest that the rSK4 channel mediates K+ secretion induced by muscarinic agonists in the rat proximal colon and that transcription of the rSK4 channel is downregulated to prevent K+ loss during dietary K+ depletion.

Chronic metabolic acid load induced by changes in dietary electrolyte balance increased chloride retention but did not compromise bone in growing swine.

The effects of chronic dietary acid loads on shifts in bone mineral reserves and physiological concentrations of cations and anions in extracellular fluids were assessed in growing swine. Four trials were conducted with a total of 38 (8.16 +/- 0.30 kg, mean +/- SEM) Large White x Landrace x Duroc pigs randomly assigned to one of three dietary treatments. Semipurified diets, fed for 13 to 17 d, provided an analyzed dietary electrolyte balance (dEB, meq/kg diet = Na+ + K+ - Cl-) of -35, 112, and 212 for the acidogenic, control, and alkalinogenic diets, respectively. Growth performance, arterial blood gas, serum chemistry, urine pH, mineral balance, bone mineral content gain, bone-breaking strength, bone ash, and percentage of bone ash were determined. Dietary treatments created a range of metabolic acid loads without affecting (P > 0.10) growth or feed intake. Urine pH was 5.71, 6.02, and 7.65 +/- 0.48 (mean +/- SEM) and arterial blood pH was 7.478, 7.485, and 7.526 +/- 0.006 for pigs fed acidogenic, control, and alkalinogenic treatments, respectively. A lower dEB resulted in an increased (P < 0.001) apparent Cl- retention (106.6, 55.4, and 41.2 +/- 6.3 meq/d), of which only 1.6% was accounted for by expansion of the extracellular fluid Cl- pool as calculated from serum Cl- (105.5, 103.4, 101.6 +/- 0.94 meq/L (mean +/- SEM) for pigs fed acidogenic, control, and alkalinogenic treatments, respectively. A lower dEB did not decrease (P > 0.10) bone mineral content gain, bone-breaking strength, bone ash, percentage of bone ash, or calcium and phosphate balance. In conclusion, bone mineral (phosphate) was not depleted to buffer the dietary acid load in growing pigs over a 3-wk period.

In rat inner medullary collecting duct, NH uptake by the Na,K-ATPase is increased during hypokalemia.

In rat terminal inner medullary collecting duct (tIMCD), the Na,K-ATPase mediates NH uptake, which increases secretion of net H(+) equivalents. K(+) and NH compete for a common binding site on the Na,K-ATPase. Therefore, NH uptake should increase during hypokalemia because interstitial K(+) concentration is reduced. We asked whether upregulation of the Na,K-ATPase during hypokalemia also increases basolateral NH uptake. To induce hypokalemia, rats ate a diet with a low K(+) content. In tIMCD tubules from rats given 3 days of dietary K(+) restriction, Na,K-ATPase beta(1)-subunit (NK-beta(1)) protein expression increased although NK-alpha(1) protein expression and Na,K-ATPase activity were unchanged relative to K(+)-replete controls. However, after 7 days of K(+) restriction, both NK-alpha(1) and NK-beta(1) subunit protein expression and Na,K-ATPase activity increased. The magnitude of Na,K-ATPase-mediated NH uptake across the basolateral membrane (J) was determined in tIMCD tubules perfused in vitro from rats after 3 days of a normal or a K(+)-restricted diet. J was the same in tubules from rats on either diet when measured at the same extracellular K(+) concentration. However, in either treatment group, increasing K(+) concentration from 10 to 30 mM reduced J >60%. In conclusion, with 3 days of K(+) restriction, NH uptake by Na,K-ATPase is increased in the tIMCD primarily from the reduced interstitial K(+) concentration.

Acute phase response and energy balance in stable human immunodeficiency virus-infected patients: a doubly labeled water study.

We sought to assess possible associations of the acute phase response with energy balance as a cause of malnutrition in uncomplicated HIV-infection. Seven stable HIV-infected patients and 7 control subjects were followed for 2 weeks for blood chemistry, body composition, total and resting energy expenditure (TEE, REE), heart rate, energy intake, and physical activity; 6 patients were investigated for interleukin-2 receptor. TEE, REE, energy intake, and anthropometric data in patients and control subjects were very similar. However, physical activity, total body potassium, and bioimpedance phase angle were decreased (1.41 +/- 0.08 vs 1.55 +/- 0.9, 152 +/- 10 g vs 191 +/- 37 g, and 6.4 +/- 0.8 degrees vs 7.1 +/- 0.5 degrees; each P < .05), and mean heart rate, fibrinogen, and erythrocyte sedimentation rate were increased in HIV-infected patients (84 +/- 6 bpm vs 76 +/- 8 bpm, 4.3 +/- 1.2 g/L vs 2.5 +/- 0.4 g/L, and 21 +/- 13 mm vs 2 +/- 3 mm; P < .05). The deviation between the measured and the predicted REE in the patient group correlated positively with heart rate and serum interleukin-2 receptor concentrations (r = 0.83 and r = 0.91; P < .05). Possible increases in REE caused by an ongoing acute phase response may be counterbalanced by reduced physical activity that results in normal TEE in HIV infection.

The absorption of iron, calcium, phosphorus, magnesium, copper and zinc in the jejunum-ileum of control and iron-deficient rats.

The effects of iron deficiency on the absorption of different dietary sources of iron were studied, together with the interactions between iron, calcium, phosphorus, magnesium, copper and zinc in the jejunum-ileum of control and iron-deficient rats. In this study, three perfusion solutions containing different iron sources: ferric citrate, haemoglobin, and equal parts of ferric citrate and haemoglobin were used. In addition, the same perfusion solutions were used with and without 2,4-dinitrophenol, an inhibitor of oxidative phosphorylation. Iron absorption in anaemic rats was greater than in the controls, except after perfusion with solutions containing haemoglobin. The absorption of calcium, copper and zinc in iron-deficient animals was not significantly affected, while the absorption of phosphorus and magnesium increased, with respect to animals in the control group. After perfusion with solutions containing haemoglobin, the absorption values of calcium, copper and zinc were lower than after ferric citrate in both groups (control and iron-deficient rats).

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.

Tratamiento de la hipertensión arterial esencial con dieta rica en potasio

Con el objetico de determinar el efecto sobre la presión arterial de una dieta rica en potasio en pacientes adultos con hipertensión arterial leve, sin modificaciones en el consumo habitual de sodio y que no se encuentren bajo tratamiento farmacológico, se estudiaron 24 pacientes, distribuidos aleatoriamente en dos grupos. Al grupo de estudio se le ordenó iuna dieta rica en potasio (alrededor de 2mEq/kg-día), durante ocho semanas. A todos los pacientes se les recomendó continuar las medidas no farmacológicas usuales. Se midió la presión arterial semanalmente en el domicilio del paciente, así como el potasio y el sodio en suero y orina al inicio y en las semanas dos,cuatro y ocho. En todos los sujetos se observó disminución en las cifras tensionales; sin embargo, la reducción de la presión arterial sistólica en el grupo de estudio fue de 7.9ñ7.99 vs 18ñ8.72 mm Hg en el control (p<0.023); mientras que la reducción en la presión diastólica fue de 8.28ñ5.89 Vs 2.86ñ4.31 mm Hg,respectivamente (p<10elevada a la - 7). El efecto sobre la presión arterial tiende a estabilizarse a partir de la cuarta semana de tratamiento. No hubo modificaciones en los niveles séricos de potasio. Se observó incremento en la excreción de potasio en el grupo de estudio de 10.09ñ25.5 vs -4.98ñ19.15 mEq/L en el control (p<0,069). Se concluye que una dieta rica en potasio contribuye favorablemente para el control de la hipertensión arterial esencial y es una medida segura en pacientes con función renal normal