Explore the vast range of titles available.

Inactivation of the tissue kallikrein gene in mice impairs renal handling of potassium due to enhanced H, K-ATPase activity, and induces hyperkalemia. We investigated whether the R53H loss-of-function polymorphism of the human tissue kallikrein gene affects renal potassium handling. In a crossover study, 30 R53R homozygous and 10 R53H heterozygous healthy males were randomly assigned to a low-sodium/high-potassium or a high-sodium/low-potassium diet to modulate tissue kallikrein synthesis. On the seventh day of each diet, participants were studied before and during a 2-h infusion of furosemide to stimulate distal potassium secretion. Urinary kallikrein activity was significantly lower in R53H than in R53R subjects on the low-sodium/high-potassium diet and was similarly reduced in both genotypes on high-sodium/low-potassium. Plasma potassium and renal potassium reabsorption were similar in both genotypes on an ad libitum sodium/potassium diet or after 7 days of a high-sodium/low-potassium diet. However, the median plasma potassium was significantly higher after 7 days of low-sodium/high-potassium diet in R53H than in R53R individuals. Urine potassium excretion and plasma aldosterone concentrations were similar. On the low-sodium/high-potassium diet, furosemide-induced decrease in plasma potassium was significantly larger in R53H than in R53R subjects. Thus, impaired tissue kallikrein stimulation by a low-sodium/high-potassium diet in R53H subjects with partial tissue kallikrein deficiency highlights an inappropriate renal adaptation to potassium load, consistent with experimental data in mice.

A dietary potassium load induces a rapid kaliuresis and natriuresis, which may occur even before plasma potassium and aldosterone (aldo) levels increase. Here we sought to gain insight into underlying molecular mechanisms contributing to this response. After gastric gavage of 2% potassium, the plasma potassium concentrations rose rapidly (0.25h), followed by a significant rise of plasma aldo (0.5h) in mice. Enhanced urinary potassium and sodium excretion was detectable as early as spot urines could be collected (about 0.5h). The functional changes were accompanied by a rapid and sustained (0.25–6h) dephosphorylation of the NaCl cotransporter (NCC) and a late (6h) upregulation of proteolytically activated epithelial sodium channels. The rapid effects on NCC were independent from the coadministered anion. NCC dephosphorylation was also aldo-independent, as indicated by experiments in aldo-deficient mice. The observed urinary sodium loss relates to NCC, as it was markedly diminished in NCC-deficient mice. Thus, downregulation of NCC likely explains the natriuretic effect of an acute oral potassium load in mice. This may improve renal potassium excretion by increasing the amount of intraluminal sodium that can be exchanged against potassium in the aldo-sensitive distal nephron.

Background and aim Hypertension is a major health problem and a risk factor for multiple diseases. In this study, we aimed to compare serum levels and the dietary intake of sodium and potassium in patients with hypertension and healthy participants of the MASHAD cohort study. Methods and design All participants of the MASHAD cohort study entered the study. Systolic blood pressure (SBP) ≥ 140 mmHg or diastolic blood pressure (DBP) ≥ 90 mmHg or a history of hypertension were defined as hypertension. Demographic variables were collected by health care professionals. Sodium and potassium dietary intake were measured using a food frequency questionnaire. Serum levels of sodium and potassium were measured using routine methods by electrolyte analyzer. Data were analyzed using SPSS version 18. Binary logistic regression model was used control for confounding factors. The significance level was set at p < 0.05. Results Of the total 9,704 participants of the Mashhad study, 6,641 participants had normal blood pressure and 3063 were hypertensive individuals. No significant difference in serum levels of sodium and potassium was observed between the two groups ( p  = 0.700, p  = 0.360 respectively). After adjusting for confounding factors, the association remained the same. Sodium and potassium dietary intake was significantly higher in the hypertensive group and after adjusting for baseline characteristics, an increase in dietary sodium intake is associated with a higher likelihood of hypertension by 0.8% (CI, 1.000-1.015). Conclusion Serum sodium and potassium levels were not associated with hypertension among MASHAD participants. Increased dietary intake of sodium was associated with hypertension even after adjusting for confounding factors.

High sodium and low potassium intakes are associated with increased levels of blood pressure and risk of cardiovascular diseases. Assessment of habitual dietary habits are helpful to evaluate their intake and adherence to healthy dietary recommendations. In this study, we determined sodium and potassium food-specific content and intake in a Northern Italy community, focusing on the role and contribution of adherence to Mediterranean diet patterns. We collected a total of 908 food samples and measured sodium and potassium content using inductively coupled plasma mass spectrometry. Using a validated semi-quantitative food frequency questionnaire, we assessed habitual dietary intake of 719 adult individuals of the Emilia-Romagna region. We then estimated sodium and potassium daily intake for each food based on their relative contribution to the overall diet, and their link to Mediterranean diet patterns. The estimated mean sodium intake was 2.15 g/day, while potassium mean intake was 3.37 g/day. The foods contributing most to sodium intake were cereals (33.2%), meat products (24.5%, especially processed meat), and dairy products (13.6%), and for potassium they were meat (17.1%, especially red and white meat), fresh fruits (15.7%), and vegetables (15.1%). Adherence to a Mediterranean diet had little influence on sodium intake, whereas potassium intake was greatly increased in subjects with higher scores, resulting in a lower sodium/potassium ratio. Although we may have underestimated dietary sodium intake by not including discretionary salt use and there may be some degree of exposure misclassification as a result of changes in food sodium content and dietary habits over time, our study provides an overview of the contribution of a wide range of foods to the sodium and potassium intake in a Northern Italy community and of the impact of a Mediterranean diet on intake. The mean sodium intake was above the dietary recommendations for adults of 1.5–2 g/day, whilst potassium intake was only slightly lower than the recommended 3.5 g/day. Our findings suggest that higher adherence to Mediterranean diet patterns has limited effect on restricting sodium intake, but may facilitate a higher potassium intake, thereby aiding the achievement of healthy dietary recommendations.

Inactivation of the B1 proton pump subunit (ATP6V1B1) in intercalated cells (ICs) leads to type I distal renal tubular acidosis (dRTA), a disease associated with salt- and potassium-losing nephropathy. Here we show that mice deficient in ATP6V1B1 (Atp6v1b1-/- mice) displayed renal loss of NaCl, K+, and water, causing hypovolemia, hypokalemia, and polyuria. We demonstrated that NaCl loss originated from the cortical collecting duct, where activity of both the epithelial sodium channel (ENaC) and the pendrin/Na(+)-driven chloride/bicarbonate exchanger (pendrin/NDCBE) transport system was impaired. ENaC was appropriately increased in the medullary collecting duct, suggesting a localized inhibition in the cortex. We detected high urinary prostaglandin E2 (PGE2) and ATP levels in Atp6v1b1-/- mice. Inhibition of PGE2 synthesis in vivo restored ENaC protein levels specifically in the cortex. It also normalized protein levels of the large conductance calcium-activated potassium channel and the water channel aquaporin 2, and improved polyuria and hypokalemia in mutant mice. Furthermore, pharmacological inactivation of the proton pump in β-ICs induced release of PGE2 through activation of calcium-coupled purinergic receptors. In the present study, we identified ATP-triggered PGE2 paracrine signaling originating from β-ICs as a mechanism in the development of the hydroelectrolytic imbalance associated with dRTA. Our data indicate that in addition to principal cells, ICs are also critical in maintaining sodium balance and, hence, normal vascular volume and blood pressure.

Background Consumption of 100% orange juice (OJ) has been positively associated with nutrient adequacy and diet quality, with no increased risk of overweight/obesity in children; however, no one has examined these factors in adults. The purpose of this study was to examine the association of 100% OJ consumption with nutrient adequacy, diet quality, and risk factors for metabolic syndrome (MetS) in a nationally representative sample of adults. Methods Data from adults 19+ years of age (n = 8,861) participating in the National Health and Nutrition Examination Survey 2003-2006 were used. The National Cancer Institute method was used to estimate the usual intake (UI) of 100% OJ consumption, selected nutrients, and food groups. Percentages of the population below the Estimated Average Requirement (EAR) or above the Adequate Intake (AI) were determined. Diet quality was measured by the Healthy Eating Index-2005 (HEI-2005). Covariate adjusted logistic regression was used to determine if consumers had a lower odds ratio of being overweight or obese or having risk factors of MetS or MetS. Results Usual per capita intake of 100% OJ was 50.3 ml/d. Among consumers (n = 2,310; 23.8%), UI was 210.0 ml/d. Compared to non-consumers, consumers had a higher (p < 0.05) percentage (% ± SE) of the population meeting the EAR for vitamin A (39.7 ± 2.5 vs 54.0 ± 1.2), vitamin C (0.0 ± 0.0 vs 59.0 ± 1.4), folate (5.8 ± 0.7 vs 15.1 ± 0.9), and magnesium (51.6 ± 1.6 vs 63.7 ± 1.2). Consumers were also more likely to be above the AI for potassium (4.1 ± 0.8 vs 1.8 ± 0.2). HEI-2005 was significantly (p < 0.05) higher in consumers (55.0 ± 0.4 vs 49.7 ± 0.3). Consumers also had higher intakes of total fruit, fruit juice, whole fruit, and whole grain. Consumers had a lower (p < 0.05) mean body mass index (27.6 ± 0.2 vs 28.5 ± 0.1), total cholesterol levels (197.6 ± 1.2 vs 200.8 ± 0.75 mg/dL), and low density lipoprotein-cholesterol levels (112.5 ± 1.4 vs 116.7 ± 0.93 mg/dL). Finally, compared to non-consumers of 100% OJ, consumers were 21% less likely to be obese and male consumers were 36% less likely to have MetS. Conclusion The results suggest that moderate consumption of 100% OJ should be encouraged to help individuals meet the USDA daily recommendation for fruit intake and as a component of a healthy diet.

This study investigated the responses to a green algae mixture of Scenedesmus dimorphus and Schroederiella apiculata (SC) containing protein (46.1% of dry algae), insoluble fibre (19.6% of dry algae), minerals (3.7% of dry algae) and omega-3 fatty acids (2.8% of dry algae) as a dietary intervention in a high carbohydrate, high fat diet-induced metabolic syndrome model in four groups of male Wistar rats. Two groups were fed with a corn starch diet containing 68% carbohydrates as polysaccharides, while the other two groups were fed a diet high in simple carbohydrates (fructose and sucrose in food, 25% fructose in drinking water, total 68%) and fats (saturated and trans fats from beef tallow, total 24%). High carbohydrate, high fat-fed rats showed visceral obesity with hypertension, insulin resistance, cardiovascular remodelling, and nonalcoholic fatty liver disease. SC supplementation (5% of food) lowered total body and abdominal fat mass, increased lean mass, and attenuated hypertension, impaired glucose and insulin tolerance, endothelial dysfunction, infiltration of inflammatory cells into heart and liver, fibrosis, increased cardiac stiffness, and nonalcoholic fatty liver disease in the high carbohydrate, high fat diet-fed rats. This study suggests that the insoluble fibre or protein in SC helps reverse diet-induced metabolic syndrome.

Renal K+ excretion is increased rapidly following dietary K+ intake, but the underlying molecular mechanisms are largely unknown. Sorensen and colleagues show that K+ intake in mice provoked rapid and near-complete dephosphorylation of the renal distal convoluted tubule NaCl cotransporter, temporally associated with increases in both Na+ and K+ excretion. This response was independent of aldosterone and may be a crucial component of the acute homeostatic adaptation of the kidney to K+ intake.

The distal nephron is composed of two main cell types: principal cells and intercalated cells. These cells have distinct morphologic features that allow them to be readily distinguished by light microscopy, as well as distinct suites of proteins that facilitate cell-specific transport properties. In this issue of the JCI, Gueutin and colleagues describe a new mechanism by which β-intercalated cells, via release of ATP and prostaglandin E2 (PGE2), influence the activity of transporters in principal cells.

Hydrochlorothiazide (HCTZ) is used to manage hypertension and heart failure; however, its side effects include mild hypokalemia, metabolic abnormalities, and volume depletion, which might have deleterious effects on renal and endothelial function. We studied whether HCTZ cause renal injury and/or altered vasoreactivity and if these changes are hypokalemia-dependent. Rats were given a normal diet or a diet moderately low in potassium (K+) with or without HCTZ. Animals fed either a low K+ diet alone or HCTZ developed mild hypokalemia. There was no significant difference in systolic blood pressure in the different treatment groups. All three groups with hypokalemia had mild proteinuria; low K+-HCTZ rats had reduced creatinine clearance. HCTZ-treated rats displayed hypomagnesemia, hypertriglyceridemia, hyperglycemia, insulin resistance, and hyperaldosteronism. No renal injury was observed in the groups without HCTZ; however, increased kidney weight, glomerular ischemia, medullary injury, and cortical oxidative stress were seen with HCTZ treatment. Endothelium-dependent vasorelaxation was reduced in all hypokalemic groups and correlated with reduced serum K+, serum, and urine nitric oxide. Our results show that HCTZ is associated with greater renal injury for the same degree of hypokalemia as the low K+ diet, suggesting that factors such as chronic ischemia and hyperaldosteronism due to volume depletion may be responsible agents. We also found impaired endothelium-dependent vasorelaxation was linked to mild hypokalemia.